Nut consumption and prostate cancer risk and mortality
Weike Wang1,6, Meng Yang2,6, Stacey A Kenfield3 , Frank B Hu1,2,4, Meir J Stampfer1,2,4, Walter C Willett1,2,4, Charles S Fuchs4,5, Edward L Giovannucci1,2,4,7 and Ying Bao*,4,7
Background: Little is known of the association between nut consumption, and prostate cancer (PCa) incidence and survivorship.
Methods: We conducted an incidence analysis and a case-only survival analysis in the Health Professionals Follow-up Study on the associations of nut consumption (updated every 4 years) with PCa diagnosis, and PCa-specific and overall mortality.
Results: In 26 years, 6810 incident PCa cases were identified from 47 299 men. There was no association between nut consumption and being diagnosed with PCa or PCa-specific mortality. However, patients who consumed nuts five or more times per week after diagnosis had a significant 34% lower rate of overall mortality than those who consumed nuts less than once per month (HR ¼ 0.66, 95% CI: 0.52–0.83, P-trend ¼ 0.0005).
Conclusions: There were no statistically significant associations between nut consumption, and PCa incidence or PCa-specific mortality. Frequent nut consumption after diagnosis was associated with significantly reduced overall mortality.
Source : British Journal of Cancer
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Association between Dietary Vitamin C Intake and Risk of Prostate Cancer: A Meta-analysis Involving 103,658 Subjects
Xiao-Yan Bai,1 Xinjian Qu,2 Xiao Jiang,1 Zhaowei Xu,1 Yangyang Yang,1 Qiming Su,2 Miao Wang,1,✉ and Huijian Wu1,2,✉
We attempted to systematically determine the association between dietary intake of vitamin C and risk of prostate cancer. PubMed and Embase were searched to obtain eligible studies published before February 2015. Cohort or case-control studies that reported the relative risk (RR)/odds ratio (OR) estimates with 95% confidence intervals (CIs) for the association between vitamin C intake and prostate cancer risk were included. Eighteen studies regarding dietary vitamin C intake were finally obtained, with a total of 103,658 subjects. The pooled RR of prostate cancer for the highest versus the lowest categories of dietary vitamin C intake was 0.89 (95%CI: 0.83-0.94; p = 0.000) with evidence of a moderate heterogeneity (I2 = 39.4%, p = 0.045). Meta-regression analysis suggested that study design accounted for a major proportion of the heterogeneity. Stratifying the overall study according to study design yielded pooled RRs of 0.92 (95%CI: 0.86-0.99, p = 0.027) among cohort studies and 0.80 (95%CI: 0.71-0.89, p = 0.000) among case-control studies, with no heterogeneity in either subgroup. In the dose-response analysis, an inverse linear relationship between dietary vitamin C intake and prostate cancer risk was established, with a 150 mg/day dietary vitamin C intake conferred RRs of 0.91 (95%CI: 0.84-0.98, p = 0.018) in the overall studies, 0.95 (95%CI: 0.90-0.99, p = 0.039) in cohort studies, and 0.79 (95%CI: 0.69-0.91, p = 0.001) in case-control studies. In conclusion, intake of vitamin C from food was inversely associated with prostate cancer risk in this meta-analysis.
Source : Journal of Cancer
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A Randomized Controlled Trial for the Effectiveness of Progressive Muscle Relaxation and Guided Imagery as Anxiety Reducing Interventions in Breast and Prostate Cancer Patients Undergoing Chemotherapy
Andreas Charalambous,1 Margarita Giannakopoulou,2 Evangelos Bozas,2 and Lefkios Paikousis3
Objective. To test the effectiveness of guided imagery (GI) and progressive muscle relaxation (PMR) as stress reducing interventions in patients with prostate and breast cancer who undergo chemotherapy.
Methods. Patients were randomly assigned to either the control group or the intervention group (PMR and GI). Patients were observed for a total duration of 3 weeks and assessed with the SAS and BECK-II questionnaires for anxiety and depression, respectively, in addiotion to two biological markers (saliva cortisol and saliva amylase) (trial registration number: NCT01275872).
Results. 256 patients were registered and 236 were randomly assigned. In total 104 were randomised to the control group and 104 to the intervention group. Intervention’s mean anxiety score and depression score changes were significantly different compared to the control’s (b=-29.4, p<0.001. b=-29.4,p<0.001 resp). Intervention group’s cortisol levels before the intervention (0.30+0.25) gradually decreased up to week 3 (0.16+0.18), whilst the control group’s cortisol levels before the intervention (0.21+0.22) gradually increased up to week 3 (0.44+0.35). The same interaction appears for the Amylase levels (p<0.001).
Conclusions. The findings showed that patients with prostate and breast cancer undergoing chemotherapy treatment can benefit from PMR and GI sessions to reduce their anxiety and depression.
Source : Evidence Based Complementary and Alternative Medicine
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Vitamin D Receptor Protein Expression in Tumor Tissue and Prostate Cancer Progression
Whitney K. Hendrickson, Richard Flavin, Julie L. Kasperzyk, Michelangelo Fiorentino, Fang Fang, Rosina Lis,
Christopher Fiore, Kathryn L. Penney, Jing Ma, Philip W. Kantoff, Meir J. Stampfer, Massimo Loda, Lorelei A. Mucci and
Purpose Data suggest that circulating 25-hydroxyvitamin D [25(OH)D] interacts with the vitamin D receptor (VDR) to decrease proliferation and increase apoptosis for some malignancies, although evidence for prostate cancer is less clear. How VDR expression in tumor tissue may influence prostate cancer progression has not been evaluated in large studies.
Patients and Methods We examined protein expression of VDR in tumor tissue among 841 patients with prostate cancer in relation to risk of lethal prostate cancer within two prospective cohorts, the Physicians' Health Study and Health Professionals Follow-Up Study. We also examined the association of VDR expression with prediagnostic circulating 25(OH)D and 1,25-dihydroxyvitamin D levels and with two VDR single nucleotide polymorphisms, FokI and BsmI.
Results Men whose tumors had high VDR expression had significantly lower prostate-specific antigen (PSA) at diagnosis (P for trend < .001), lower Gleason score (P for trend < .001), and less advanced tumor stage (P for trend < .001) and were more likely to have tumors harboring the TMPRSS2:ERG fusion (P for trend = .009). Compared with the lowest quartile, men whose tumors had the highest VDR expression had significantly reduced risk of lethal prostate cancer (hazard ratio [HR], 0.17; 95% CI, 0.07 to 0.41). This association was only slightly attenuated after adjustment for Gleason score and PSA at diagnosis (HR, 0.33; 95% CI, 0.13 to 0.83) or, additionally, for tumor stage (HR, 0.37; 95% CI, 0.14 to 0.94). Neither prediagnostic plasma vitamin D levels nor VDR polymorphisms were associated with VDR expression.
Conclusion High VDR expression in prostate tumors is associated with a reduced risk of lethal cancer, suggesting a role of the vitamin D pathway in prostate cancer progression.
Source : Journal of Clinical Oncology
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Cranberry Supplements May Reduce the Severity of Radiation-induced Cystitis
Hamilton K, Bennett NC, Purdie G, Herst PM. Standardized cranberry capsules for radiation cystitis in prostate cancer patients in New Zealand: a randomized double blinded, placebo controlled pilot study. Support Care Cancer. July 2014; [epub ahead of print]. doi: 10.1007/s00520-014-2335-8.
Patients with prostate cancer undergoing radiation therapy often experience acute radiation-induced cystitis (inflammation of the bladder). Although the symptoms of this condition can be treated, there are no preventative therapies available. Cranberry (Vaccinium macrocarpon) supplements have been associated with urinary tract health and therefore may beneficial for patients with radiation-induced cystitis. The aim of this double-blinded, randomized, placebo-controlled pilot trial was to evaluate the effects of a standardized cranberry supplement on the incidence and severity of radiation cystitis in patients with prostate cancer.
The men participating in this study received radiation therapy for their prostate and regional lymph nodes at theSouthern Blood and Cancer Centre in Dunedin, New Zealand. Eligible patients were identified from planning computed tomography (CT) scans that assessed the prostate, bladder, and bowel. Excluded patients included men who had previous radiation therapy, metastatic disease, consumed warfarin, had a Karnofsky performance status score <70 (required at least some assistance for personal care), had kidney stones, or an allergy to cranberries.
In terms of radiation treatment, the patients were prescribed a dose of 74 Gy in 37 fractions or 64 Gy in 32 fractions to the prostate and prostate bed, respectively. The patients all received intensity-modulated radiation therapy (6MV photon beam). Radiation treatment was directed to the prostate, prostate bed, and/or regional lymph nodes. There was a 9-week radiation treatment period for prostate bed and 10-week treatment for prostate and prostate nodes. Patients (n=41) were randomly assigned to take a capsule a day (during breakfast) of either a cranberry extract (n=20) or a placebo (n=21) (Naturo Pharm LTD; Rotorua, New Zealand) during the entire radiation treatment period and 2 weeks post-treatment. The cranberry capsules contained 72 mg proanthocyanidins (PACs), determined by UV-VISEP/CN standard method, and the placebo capsules were nearly identical in taste, color, and smell to the capsules with the cranberry extracts.
Patients were advised not to consume or limit the consumption of wine, grapes (Vitis vinifera), cranberries, or other berries during the study. Treatment effects were evaluated by assessing the Modified Expanded Prostate Index Composite (EPIC) scores both at the beginning and the end of the study. In particular, this study focused on 5 urinary symptoms and the degree that 7 urinary tract symptoms bothered the patients.
The results of this study were analyzed on an intent-to-treat basis for 40 patients (20 in both groups). A total of 2 patients did not comply with the study, including 1 that left the study after 2 weeks. Most of the men (mean age: 68 years) in this study were of European descent (93%) and had a mid-range Gleason score (grading system for prostate cancer) of 6 or 7. In addition, nearly half of the patients had stage T1 disease (beginning of disease). Furthermore, all patient-related factors were evenly distributed between the 2 groups.
Based on symptom scoring, the researchers found that the incidence of cystitis was 65% for the patients in the cranberry treatment group and 90% for the patients in the placebo group (P=0.058). Moreover, 30% of the patients in the cranberry group and 45% of the patients in the placebo group had severe cystitis (P=0.30). There were no men in the study that developed a urinary tract infection (UTI). All EPIC scores were consistently lower for the cranberry cohort. In particular, the cranberry cohort had significantly lower mean (P=0.045) and maximum (P=0.019) scores for pain/burning urination symptoms. The cranberry cohort also had better mean scores for urine stream, although this was not significant when accounting for baseline symptoms (P=0.14).
Patients that presented with baseline urinary symptoms had worse EPIC scores for most symptoms. Less pain/burning (P=0.042), better control (P=0.034), stronger urine stream (P=0.036), and less leaking/dribbling (P=0.024), in comparison to the placebo group, were found to be significant only in the cranberry treatment group with baseline urinary symptoms. Additionally, patients in the cranberry cohort that followed the low hydration regimen had significant effects on symptoms for pain/burning (P=0.038), stronger urine stream (P=0.038), and less use of pad/liners (P=0.042). There were no significant differences found in the high hydration regimen.
The authors conclude, "Men receiving radiation therapy for prostate cancer may benefit from using cranberry capsules, particularly those on low hydration regimens or presenting with urinary symptoms before radiation treatment." Although the results are promising, one of the limitations of this study was that the improvements were based only on a questionnaire. This study could also have evaluated inflammation markers or any other diagnostic features of cystitis. Despite this shortcoming, the interesting results of this pilot study warrant further investigations on the use of cranberry supplements for radiation-induced cystitis.
--Laura M. Bystrom, PhD
Source : American Botanical Council
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Dairy products, calcium, and prostate cancer risk: a systematic review and meta-analysis of cohort studies1,2,3,4
- Dagfinn Aune,
- Deborah A Navarro Rosenblatt,
- Doris SM Chan,
- Ana Rita Vieira,
- Rui Vieira,
- Darren C Greenwood,
- Lars J Vatten, and
- Teresa Norat
Background: Dairy product and calcium intakes have been associated with increased prostate cancer risk, but whether specific dairy products or calcium sources are associated with risk is unclear.
Objective: In the Continuous Update Project, we conducted a meta-analysis of prospective studies on intakes of dairy products and calcium and prostate cancer risk.
Design: PubMed and several other databases were searched up to April 2013. Summary RRs were estimated by using a random-effects model.
Results: Thirty-two studies were included. Intakes of total dairy products [summary RR: 1.07 (95% CI: 1.02, 1.12; n = 15) per 400 g/d], total milk [summary RR: 1.03 (95% CI: 1.00, 1.07; n = 14) per 200 g/d], low-fat milk [summary RR: 1.06 (95% CI: 1.01, 1.11; n = 6) per 200 g/d], cheese [summary RR: 1.09 (95% CI: 1.02, 1.18; n = 11) per 50 g/d], and dietary calcium [summary RR: 1.05 (95% CI: 1.02, 1.09; n = 15) per 400 mg/d] were associated with increased total prostate cancer risk. Total calcium and dairy calcium intakes, but not nondairy calcium or supplemental calcium intakes, were also positively associated with total prostate cancer risk. Supplemental calcium was associated with increased risk of fatal prostate cancer.
Conclusions: High intakes of dairy products, milk, low-fat milk, cheese, and total, dietary, and dairy calcium, but not supplemental or nondairy calcium, may increase total prostate cancer risk. The diverging results for types of dairy products and sources of calcium suggest that other components of dairy rather than fat and calcium may increase prostate cancer risk. Any additional studies should report detailed results for subtypes of prostate cancer.
Source : Amercan Journal of Clinical Nutrition
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Dietary intakes of carbohydrates in relation to prostate cancer risk: a prospective study in the Malmö Diet and Cancer cohort1,2,3
- Isabel Drake,
- Emily Sonestedt,
- Bo Gullberg,
- Göran Ahlgren,
- Anders Bjartell,
- Peter Wallström, and
- Elisabet Wirfält
Background: Dietary carbohydrates have been implicated in relation to prostate cancer.
Objective: Our objective was to examine the associations between dietary intakes of carbohydrates, fiber, and their food sources and risk of prostate cancer, overall and by case severity, in the Malmö Diet and Cancer cohort.
Design: The analysis included 8128 men aged 45–73 y without a history of cancer, cardiovascular disease, or diabetes and who were classified as adequate energy reporters. After a median follow-up time of 15 y, prostate cancer was diagnosed in 817 men. We used Cox proportional hazards regression to model associations between energy-adjusted nutrient and food intakes with risk of incident prostate cancer, with competing risk of death from non–prostate cancer causes taken into account.
Results: After adjustment for age and other known or potential risk factors, we observed no associations between total carbohydrates or dietary fiber and prostate cancer. We observed positive associations between the intake of low-fiber cereals with overall and low-risk prostate cancer and between intakes of cake and biscuits and rice and pasta with low-risk prostate cancer (all P-trend < 0.05). A high intake compared with zero consumption of sugar-sweetened beverages was associated with increased risk of symptomatic prostate cancer (HR: 1.38; 95% CI: 1.04, 1.84).
Conclusions: Results from this large study with high-validity dietary data suggest that a high intake of refined carbohydrates may be associated with increased risk of prostate cancer. However we observed no significant associations with high-risk prostate cancer, and not all foods that are typically high in refined carbohydrates were associated with prostate cancer.
Source : The American Journal of Clinical Nutrition
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Coffee consumption and risk of prostate cancer: an up-to-date meta-analysis
S Zhong1, W Chen2, X Yu3, Z Chen4, Q Hu5 and J Zhao1
- 1Center of Clinical Laboratory Science, Jiangsu Cancer Hospital Affiliated to Nanjing Medical University, Nanjing, China
- 2The Fourth Clinical College of Nanjing Medical University, Nanjing, China
- 3Department of Hematology (Key Department of Jiangsu Medicine), Zhongda Hospital, Medical School, Southeast University, Nanjing, China
- 4Department of General Surgery, The Affiliated Hospital of Xuzhou Medical College, Xuzhou, China
- 5Teaching and Research Office of General Surgery, Xuzhou Medical College, Xuzhou, China
Background/Objectives: Epidemiologic findings concerning the association between coffee consumption and prostate cancer risk yielded mixed results. We aimed to investigate the association by performing a meta-analysis of all available studies.
Subjects/Methods: We searched PubMed, Web of Science and EMBASE for studies published up to July 2013. We calculated the summary relative risk (RR) and 95% confidence intervals (CIs) for ever, moderate and highest consumption of coffee vs non/lowest consumption. The dose–response relationship was assessed by restricted cubic spline model and multivariate random-effect meta-regression.
Results: A total of 12 case–control studies and 12 cohort studies with 42 179 cases were selected for final meta-analysis. No significant associations were found among overall analysis. A borderline positive association was found for highest drinkers in five small hospital-based case–control (HCC) studies involving 2278 cases. However, compared with non/lowest drinkers, the summary RRs were 0.92 (95% CI=0.85–0.99) for ever drinkers, 0.92 (95% CI=0.85–1.00) for moderate drinkers and 0.83 (95% CI=0.72–0.96) for highest drinkers from 12 cohort studies, comprising a total of 34 424 cases. An increase in coffee intake of two cups/day was associated with a 7% decreased risk of prostate cancer according to cohort studies. A significant inverse relationship was also found for fatal prostate cancers and high-grade prostate cancers.
Conclusions: Case–control studies especially HCC ones might be prone to selection bias and recall bias that might have contributed to the conflicting results. Therefore, the present meta-analysis suggests a borderline significant inverse association between coffee consumption and prostate cancer risk based on cohort studies.
Source : EU Journal of Clinical Nutrition
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Apigenin inhibits prostate cancer progression in TRAMP mice via targeting PI3K/Akt/FoxO pathway
- Sanjeev Shukla1,
- Natarajan Bhaskaran1,
- Melissa A. Babcook1,2,
- Pingfu Fu3,
- Gregory T. MacLennan4 and
- Sanjay Gupta1,2,5,*
Forkhead box O (FoxO) transcription factors play an important role as tumor suppressor in several human malignancies. Disruption of FoxO activity due to loss of phosphatase and tensin homolog and activation of phosphatidylinositol-3 kinase (PI3K)/Akt are frequently observed in prostate cancer. Apigenin, a naturally occurring plant flavone, exhibits antiproliferative and anticarcinogenic activities through mechanisms, which are not fully defined. In the present study, we show that apigenin suppressed prostate tumorigenesis in transgenic adenocarcinoma of the mouse prostate (TRAMP) mice through the PI3K/Akt/FoxO-signaling pathway. Apigenin-treated TRAMP mice (20 and 50 μg/mouse/day, 6 days/week for 20 weeks) exhibited significant decrease in tumor volumes of the prostate as well as completely abolished distant organ metastasis. Apigenin treatment resulted in significant decrease in the weight of genitourinary apparatus (P < 0.0001), dorsolateral (P < 0.0001) and ventral prostate (P < 0.028), compared with the control group. Apigenin-treated mice showed reduced phosphorylation of Akt (Ser473) and FoxO3a (Ser253), which correlated with its increased nuclear retention and decreased binding of FoxO3a with 14-3-3. These events lead to reduced proliferation as assessed by Ki-67 and cyclin D1, along with upregulation of FoxO-responsive proteins BIM and p27/Kip1. Complementing in vivo results, similar observations were noted in human prostate cancer LNCaP and PC-3 cells after apigenin treatment. Furthermore, binding of FoxO3a with p27/Kip1 was markedly increased after 10 and 20 μM apigenin treatment resulting in G0/G1-phase cell cycle arrest, which was consistent with the effects elicited by PI3K/Akt inhibitor, LY294002. These results provide convincing evidence that apigenin effectively suppressed prostate cancer progression, at least in part, by targeting the PI3K/Akt/FoxO-signaling pathway.
Source : Carcinogenesis
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Coffee consumption and risk of prostate cancer: a meta-analysis of prospective cohort studies
Observational studies and animal evidence suggest an association between coffee consumption and the risk of prostate cancer. However, the results are inconsistent. We evaluated the association by conducting a meta-analysis of prospective cohort studies. PubMed and Embase were searched through June 2013 to identify studies that met predetermined inclusion criterion. A random-effects model was used to calculate the pooled risk estimates. Ten prospective cohort studies involving 8973 patients with prostate cancer and 206 096 participants were included in this systematic review. Compared with individuals who seldom or never drink coffee, the pooled relative risk of prostate cancer was 0.88 (95% confidence interval: 0.82–0.95) for regular coffee drinkers. Exclusion of any single study did not materially alter the combined risk estimate. Visual inspection of a funnel plot and Begg’s and Egger’s tests did not indicate evidence of publication bias. In summary, integrated evidence from prospective cohort studies supports the hypothesis that coffee consumption may decrease the risk of prostate cancer.
Source : Carcinogenesis
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_Active Component of Grape Seed Extract Effective Against Cancer Cells
A University of Colorado Cancer Center study published online ahead of print in the journal Nutrition and Cancer describes the laboratory synthesis of the most active component of grape seed extract, B2G2, and shows this synthesized compound induces the cell death known as apoptosis in prostate cancer cells while leaving healthy cells unharmed.
"We've shown similar anti-cancer activity in the past with grape seed extract (GSE), but now we know B2G2 is its most biologically active ingredient which can be synthesized in quantities that will allow us to study the detailed death mechanism in cancer cells," says Alpna Tyagi, PhD, of the University of Colorado Skaggs School of Pharmacy and Pharmaceutical Sciences. Tyagi works in the lab of CU Cancer Center investigator and Skaggs School of Pharmacy faculty member, Chapla Agarwal, PhD.
The group has spent more than a decade demonstrating the anti-cancer activity of GSE in controlled, laboratory conditions. For example, previous studies have shown the GSE effectiveness against cancer cells and have also shown its mechanism of action. "But until recently, we didn't know which constituent of GSE created this effect. This naturally occurring compound, GSE, is a complex mixture of polyphenols and also so far it has been unclear about the biologically active constituents of GSE against cancer cells," Tyagi says.
Eventually the group pinpointed B2G2 as the most active compound, but, "it's expensive and it takes a long time to isolate B2G2 from grape seed extract," Tyagi says.
This expense related to the isolation of B2G2 has limited the group's further exploration. So instead of purifying B2G2 from GSE, the group decided to synthesize it in the lab. The current study reports the success of this effort, including the ability to synthesize gram-quantity of B2G2 reasonably quickly and inexpensively.
In the paper's second half, the group shows anti-cancer activity of synthesized B2G2 similar in mechanism and degree to overall GSE effectiveness.
"Our goal all along has been a clinical trial of the biologically active compounds from GSE against human cancer. But it's difficult to earn FDA approval for a trial in which we don't know the mechanisms and possible effects of all active components. Therefore, isolating and synthesizing B2G2 is an important step because now we have the ability to conduct more experiments with the pure compound. Ongoing work in the lab further increases our understanding of B2G2's mechanism of action that will help for the preclinical and clinical studies in the future," Tyagi says.
Source : PRWeb
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Four or More Cups of Coffee a Day May Keep Prostate Cancer Recurrence and Progression Away
Bioactive compounds in coffee may have anti-inflammatory and antioxidant effects
Coffee consumption is associated with a lower risk of prostate cancer recurrence and progression, according to a new study by Fred Hutchinson Cancer Research Center scientists that is online ahead of print in Cancer Causes & Control. Corresponding author Janet L. Stanford, Ph.D., co-director of the Program in Prostate Cancer Research in the Fred Hutch Public Health Sciences Division, conducted the study to determine whether the bioactive compounds in coffee and tea may prevent prostate cancer recurrence and delay progression of the disease.
Stanford and colleagues found that men who drank four or more cups of coffee per day experienced a 59 percent reduced risk of prostate cancer recurrence and/or progression as compared to those who drank only one or fewer cups per week.
They did not, however, find an association between coffee drinking and reduced mortality from prostate cancer, although the study included too few men who died of prostate cancer to address that issue separately.
First study to assess the link between tea and prostate cancer outcomes
Regarding tea consumption, the researchers did not find an associated reduction of prostate cancer recurrence and/or progression. The study also did not draw any conclusions regarding the impact of tea drinking on prostate-specific death.
“To our knowledge, our study is the first to investigate the potential association between tea consumption and prostate cancer outcomes,” the authors wrote. “It is important to note, however, that few patients in our cohort were regular tea drinkers and the highest category of tea consumption was one or more cups per day. The association should be investigated in future studies that have access to larger populations with higher levels of tea consumption.”
The population-based study involved 1,001 prostate cancer survivors, aged 35-74 years old at the time of diagnosis between 2002-2005, who were residents of King County, Wash. Participants answered questions regarding their diet and beverage consumption two years prior to prostate cancer diagnosis using a validated food frequency questionnaire, and were interviewed about demographic and lifestyle information, family history of cancer, medication use and prostate cancer screening history.
The researchers followed up with patients more than five years after diagnosis to ascertain whether the prostate cancer had recurred and/or progressed. Those who were still living, willing to be contacted and had been diagnosed with non-metastatic cancer were included in the follow-up effort.
Of the original 1,001 patients in the cohort, 630 answered questions regarding coffee intake, fit the follow-up criteria and were included in the final analysis. Of those, 61 percent of the men consumed at least one cup of coffee per day and 12 percent consumed the highest amount: four or more cups per day.
The study also evaluated daily coffee consumption in relation to prostate cancer-specific death in 894 patients using data from the initial food frequency questionnaire. After the median follow-up period of eight-and-a-half years, 125 of the men had died, including 38 specifically from prostate cancer. Daily coffee consumption was not associated with prostate cancer-specific mortality or other-cause mortality, but with few deaths these analyses were limited.
“Our study differs from previous ones because we used a composite definition of prostate cancer recurrence/progression,” said first author Milan Geybels, a doctoral student at Maastricht University in the Netherlands who was a graduate student in Stanford’s Prostate Studies group at Fred Hutch when the study was conducted. “We used detailed information on follow-up prostate-specific antigen levels, use of secondary treatment for prostate cancer and data from scans and biopsies to assess occurrence of metastases and cause-specific mortality during follow up. Using these detailed data, we could determine whether a patient had evidence of prostate cancer recurrence or progression.”
The results are consistent with findings from Harvard’s Health Professionals Follow-up Study, which found that men who drank six or more cups of coffee per day had a 60 percent decreased risk of metastatic/lethal prostate cancer as compared to coffee abstainers.
Phytochemicals in coffee have anti-inflammatory and antioxidant effects
Further research is required to understand the mechanisms underlying the results of the study, but biological activities associated with consumption of phytochemical compounds found in coffee include anti-inflammatory and antioxidant effects and modulation of glucose metabolism. These naturally occurring compounds include:
• Caffeine, which has properties that inhibit cell growth and encourage apoptosis, or programmed cell death. Previous studies have found that caffeine consumption may reduce the risk of several cancer types, including basal-cell carcinoma, glioma (a cancer of the brain and central nervous system) and ovarian cancer.
• Diterpenes cafestol and kahweol, which may inhibit cancer growth.
• Chlorogenic acid, which, along with caffeic acid, can inhibit DNA methylation, a biochemical process involved in the development and progression of many cancer types.
Additional studies needed to confirm whether coffee can prevent cancer recurrence
The researchers emphasize that coffee or specific coffee components cannot be recommended for secondary prevention of prostate cancer before the preventive effect has been demonstrated in a randomized clinical trial. Further, there’s ongoing debate about which components in coffee are anti-carcinogenic, and additional large, prospective studies are needed to confirm whether coffee intake is beneficial for secondary prevention.
Coffee drinking may even be problematic for some men, Geybels said.
“Although coffee is a commonly consumed beverage, we have to point out that increasing one’s coffee intake may be harmful for some men. For instance, men with hypertension may be vulnerable to the adverse effects of caffeine in coffee. Or, specific components in coffee may raise serum cholesterol levels, posing a possible threat to coronary health. Patients who have questions or concerns about their coffee intake should discuss them with their general practitioner,” he said.
The investigators also noted limits to their study, which included a lack of data on how coffee consumption might have changed following diagnosis, whether the coffee that participants consumed was caffeinated or decaffeinated, and how the coffee was prepared (espresso, boiled or filtered), a factor that may affect the bioactive properties of the brew.
Source : Newswise
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Study Shows How Vitamin E Can Help Prevent Cancer
COLUMBUS, Ohio – Researchers have identified an elusive anti-cancer property of vitamin E that has long been presumed to exist, but difficult to find.
Many animal studies have suggested that vitamin E could prevent cancer, but human clinical trials following up on those findings have not shown the same benefits.
In this new work, researchers showed in prostate cancer cells that one form of vitamin E inhibits the activation of an enzyme that is essential for cancer cell survival. The loss of the enzyme, called Akt, led to tumor cell death. The vitamin had no negative effect on normal cells.
“This is the first demonstration of a unique mechanism of how vitamin E can have some benefit in terms of cancer prevention and treatment,” said lead author Ching-Shih Chen, professor of medicinal chemistry and pharmacognosy at The Ohio State University and an investigator in Ohio State’s Comprehensive Cancer Center.
The study appears in the March 19, 2013, issue of the journal Science Signaling.
Chen cautioned that taking a typical vitamin E supplement won’t offer this benefit for at least two reasons: The most affordable supplements are synthetic and based predominantly on a form of the vitamin that did not fight cancer as effectively in this study, and the human body can’t absorb the high doses that appear to be required to achieve the anti-cancer effect.
“Our goal is to develop a safe pill at the right dose that people could take every day for cancer prevention. It takes time to optimize the formulation and the dose,” he said.
Chen has filed an invention disclosure with the university, and Ohio State has filed a patent application for the agent.
Vitamin E occurs in numerous forms based on their chemical structure, and the most commonly known form belongs to a variety called tocopherols. In this study, researchers showed that, of the tocopherols tested, the gamma form of tocopherol was the most potent anti-cancer form of the vitamin.
The scientists manipulated the structure of that vitamin E molecule and found that the effectiveness of this new agent they created was 20-fold higher than the vitamin itself in cells. In experiments in mice, this agent reduced the size of prostate cancer tumors.
These findings suggest that an agent based on the chemical structure of one form of vitamin E could help prevent and treat numerous types of cancer – particularly those associated with a mutation in the PTEN gene, a fairly common cancer-related genetic defect that keeps Akt active.
The researchers began the work with both alpha and gamma forms of the vitamin E molecule. Both inhibited the enzyme called Akt in very targeted ways, but the gamma structure emerged as the more powerful form of the vitamin.
In effect, the vitamin halted Akt activation by attracting Akt and another protein, called PHLPP1, to the same region of a cell where the vitamin was absorbed: the fat-rich cell membrane. PHLPP1, a tumor suppressor, then launched a chemical reaction that inactivated Akt, rendering it unable to keep cancer cells alive.
“This is a new finding. We have been taking vitamin E for years but nobody really knew about this particular anti-cancer mechanism,” Chen said.
The gamma form was most effective because its chemical shape allowed it to attach to Akt in the most precise way to shut off the enzyme.
Because of how the various molecules interacted on the cell membrane, the scientists predicted that shortening a string of chemical groups dangling from the main body, or head group, of the gamma-tocopherol molecule would make those relationships even stronger. They lopped off about 60 percent of this side chain and tested the effects of the new agent in the prostate cancer cells.
“By reducing two-thirds of the chain, the molecule had a 20 times more potent anti-tumor effect, while retaining the integrity of vitamin E’s head group,” Chen said. This manipulation enhanced the anti-tumor potency of the molecule by changing its interaction with the cell membrane, so that the head group was more accessible to Akt and PHLPP1.
When mice with tumors created by these two prostate cancer cell lines were inSource : jected with the agent, the treatment suppressed tumor growth when compared to a placebo, which had no effect on tumor size. Chemical analysis of the treated tumors showed that the Akt enzyme signal was suppressed, confirming the effects were the same in animals as they had been in cell cultures.
The animal study also suggested the experimental agent was not toxic. Chen’s lab is continuing to work on improvements to the molecule.
Source : Ohio State University
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Green Tea Reduced Inflammation, May Inhibit Prostate Cancer Tumor Growth, Research Finds
Men with prostate cancer who consumed green tea prior to undergoing prostatectomy had reductions in markers of inflammation, according to data presented at the 11th Annual AACR International Conference on Frontiers in Cancer Prevention Research, held in Anaheim, Calif., Oct. 16-19, 2012.
"Our study showed that drinking six cups of green tea affected biomarkers in prostate tissue at the time of surgery," said Susanne M. Henning, Ph.D., R.D., adjunct professor at the David Geffen School of Medicine at the University of California Los Angeles. "This research offers new insights into the mechanisms by which green tea consumption may reduce the risk for prostate cancer by opposing processes such as inflammation, which are associated with prostate cancer growth."
Prior epidemiological data have been inconclusive about the relationship between green tea and prostate cancer. However, one recent intervention study conducted in Italy revealed that men with a precursor to prostate cancer called prostatic intraepithelial neoplasia who consumed a green tea extract reduced their risk for progression to prostate cancer.
Henning and colleagues examined potential mechanisms by which green tea may have beneficial effects among 67 men with prostate cancer scheduled to undergo prostatectomy. The researchers randomly assigned the men to either six cups of brewed green tea or water daily for three to eight weeks, depending on the timing of their surgery. They collected blood and urine samples before and after the green tea or water consumption and collected prostate tissue following the pathology exam.
The data showed that serum prostate-specific antigen (PSA) concentrations were significantly lower at the end of the study compared with baseline levels in men consuming green tea. In addition, prostate tissue PSA protein expression was lower in men assigned to green tea consumption compared with the control group at the end of the study.
Further, immunostaining analysis revealed that nuclear factor kappa B, a marker of inflammation, was significantly reduced in those men assigned to green tea compared with those in the control group. A urinary marker of oxidative DNA damage was significantly decreased in urine from men consuming green tea compared with controls.
The researchers found no differences in markers of tumor cell proliferation between the two treatment groups.
Henning and her colleagues are further evaluating the association between green tea and prostate cancer by trying to enhance its activity. Currently, they are exploring the possibility of combining green tea with other natural products in mouse studies.
Source : Science Daily
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VITAMIN E AND PROSTATE CANCER IN HEALTHY MEN
A paper published recently from the Selenium and Vitamin E Cancer Prevention Trial (SELECT) in the Journal of the American Medical Association (JAMA 306:1549-1556, 2011) concluded that "dietary supplementation with vitamin E significantly increased the risk of prostate cancer among healthy men." This alarming news spread fast, and many men are now wondering if it is prudent to take vitamin E supplements in light of this new information.
To date, two large randomized, placebo-controlled trials (RCTs) have been conducted in healthy men to investigate the effect of vitamin E supplementation on prostate cancer: The Physicians' Health Study (PHS) II and SELECT. PHS II (JAMA 301:52-62, 2009) followed 14,641 healthy men, aged 50 years and older, given 400 International Units (IU) of synthetic vitamin E every other day for eight years. In SELECT, 35,533 healthy men, aged 50 and older, received 400 IU of synthetic vitamin E every day for seven years. In both trials, there was no benefit of taking vitamin E supplements on prostate cancer risk. After a median time of 5.5 years in SELECT, vitamin E supplementation was discontinued, yet followup of the study participants continued for 1.5 years in order to document additional events. Unexpectedly, the SELECT updated analysis published recently in JAMA found a 17% increased risk of being diagnosed with prostate cancer in men who had taken the vitamin E supplement compared to those who had received placebo. No biological mechanism was proposed to explain the increased incidence of prostate cancer.
Why Did They Look at Vitamin E in the First Place? Vitamin E functions as a powerful, fat-soluble antioxidant in our cells and tissues. Antioxidants neutralize the effects of free radicals, highly reactive species that oxidize DNA, proteins, and lipids inside our cells, potentially causing damage and contributing to disease. In particular, oxidative DNA damage may cause mutations and, hence, increase the risk of certain cancers, including prostate cancer. Free-radical exposure is an unavoidable aspect of our lives, as these radicals are produced as a natural by-product of many biological processes, such as cellular respiration and inflammation, in addition to coming from our environment, particularly cigarette smoke. Antioxidants produced in the body and ingested in the diet are essential to reduce oxidative stress and counteract the potentially harmful effects of free radicals.
Some studies support a beneficial role for vitamin E in cancer and cardiovascular disease prevention. For example, the Women's Health Study (JAMA 294:56-65, 2005) followed 39,876 women who took 600 IU natural vitamin E every other day for ten years. The investigators found that supplemental vitamin E decreased cardiovascularrelated deaths by 24% but had no effect on cardiovascular Vitamin E and Prostate Cancer in Healthy Men events, overall cancer incidence, or cancer-related deaths. In general, studies have reported mixed results, and the impact of vitamin E supplementation on chronic disease risk remains controversial.
Why Are the Results Different? The Women's Health Study (WHS), PHS II, and SELECT are RCTs, also referred to as clinical trials or intervention studies. In RCTs, individuals are randomly assigned to either treatment (vitamin E in this case) or placebo, and the impact of the intervention on disease incidence is evaluated after several years.
The important issues that emerge from these RCTs are vitamin E dose (200-400 IU/day), vitamin E form (natural vs. synthetic), and population studied. Synthetic vitamin E (all-rac-alpha-tocopherol or dl-alpha-tocopherol) has half the bioactivity of naturally occurring vitamin E (RRR-alpha-tocopherol or d-alpha-tocopherol)—hence, the "effective dose" in PHS II and SELECT was only 100 and 200 IU/day, respectively, and 300 IU/day in WHS. Higher doses may be needed to effectively reduce oxidative stress. In one dose-response study, significant reductions in plasma F2-isoprostanes (a marker of oxidative stress) occurred only at daily doses of at least 1,600 IU of natural-source vitamin E. Notably, this dose is above the tolerable upper intake level (UL) of 1,500 IU/day set by the Food and Nutrition Board of the Institute of Medicine.
The fact that the vitamin E doses used in the RCTs appear insufficient to lower oxidative stress may explain the lack of benefit with respect to cancer risk. It remains unknown whether oxidative stress plays a causal role in prostate cancer. Furthermore, it remains unexplained why vitamin E supplementation in SELECT was associated with a 17% increased risk of prostate cancer, whereas vitamin E supplementation in PHS II and WHS was not associated with increased risk of any type of cancer in men and women, respectively.
Finally, the population studied in SELECT was healthy males consuming a well-balanced diet, most of whom likely were not vitamin E deficient or under increased oxidative stress. Unfortunately, neither baseline vitamin E levels in the study participants’ blood nor their oxidative stress status was assessed. In situations of stress, disease, or deficiency, meeting an increased demand with vitamin E supplementation may be warranted. However, in healthy people, vitamin E supplementation shows no added benefit on disease risk, as confirmed by the RCTs discussed here. For example, a study on the effect of supplemental vitamin E on cancer risk in 29,000 Finnish male smokers (the Alpha-Tocopherol Beta-Carotene [ATBC] trial) reported in 1998 that daily supplements of 75 IU/day of synthetic vitamin E for five to eight years were associated with a 32% and 41% reduction in prostate cancer diagnosis and mortality, respectively, compared to unsupplemented smokers. However, among other limitations, the ATBC study was not designed to assess prostate cancer incidence as a primary endpoint. Since oxidative stress was not measured in the study subjects, the mechanism for the possible protective effect of low-dose vitamin E remains obscure. Factors other than oxidative stress play an important role in the etiology of prostate cancer, such as endogenous hormones, race, age, and dietary fat intake.
Based on the lack of conclusive evidence for a benefit of vitamin E supplementation in cancer and cardiovascular disease prevention in generally healthy adults and the potential for harm in certain subpopulations, the Linus Pauling Institute has revised its "Rx for Health" and no longer includes a recommendation for supplemention with 200 IU/day of natural-source vitamin E.
What to Do? Vitamin E is an important micronutrient, and meeting daily recommendations is critical for optimum health. The Recommended Dietary Allowance (RDA) of vitamin E for adult men and women is 22.5 IU per day. Notably, more than 90% of individuals aged 2 years and older in the U.S. do not meet the daily requirement for vitamin E from food sources alone. Major sources of vitamin E in the American diet are vegetable oils, nuts, whole grains, and green leafy vegetables.
Taking all the issues discussed above into consideration, LPI recommends that generally healthy adults take a daily multivitamin/mineral supplement, which usually contains 30 IU of synthetic vitamin E, or 90% of the RDA.
Source : Linus Pauling Institute
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Benefits of whole ginger extract in Prostate cancer
Prasanthi Karnaa1, Sharmeen Chagania1, Sushma R. Gundalaa1, Padmashree C. G. Ridaa1, Ghazia Asifa1, Vibhuti Sharmaa1, Meenakshi V. Guptaa2 and Ritu Anejaa1 c1
a1 Department of Biology, Georgia State University, Atlanta, GA 30303, USA
a2 West Georgia Hospitals, LaGrange, GA 30240, USA
It is appreciated far and wide that increased and regular consumption of fruits and vegetables is linked with noteworthy anticancer benefits. Extensively consumed as a spice in foods and beverages worldwide, ginger (Zingiber officinale Roscoe) is an excellent source of several bioactive phenolics, including non-volatile pungent compounds such as gingerols, paradols, shogaols and gingerones. Ginger has been known to display anti-inflammatory, antioxidant and antiproliferative activities, indicating its promising role as a chemopreventive agent. Here, we show that whole ginger extract (GE) exerts significant growth-inhibitory and death-inductory effects in a spectrum of prostate cancer cells. Comprehensive studies have confirmed that GE perturbed cell-cycle progression, impaired reproductive capacity, modulated cell-cycle and apoptosis regulatory molecules and induced a caspase-driven, mitochondrially mediated apoptosis in human prostate cancer cells. Remarkably, daily oral feeding of 100 mg/kg body weight of GE inhibited growth and progression of PC-3 xenografts by approximately 56 % in nude mice, as shown by measurements of tumour volume. Tumour tissue from GE-treated mice showed reduced proliferation index and widespread apoptosis compared with controls, as determined by immunoblotting and immunohistochemical methods. Most importantly, GE did not exert any detectable toxicity in normal, rapidly dividing tissues such as gut and bone marrow. To the best of our knowledge, this is the first report to demonstrate the in vitro and in vivo anticancer activity of whole GE for the management of prostate cancer.
Source : British Journal of Nutrition
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A high-fat diet containing whole walnuts (juglans regia) reduces tumour size and growth along with plasma insuling-like growth factor 1 in the transgenic adencarcinoma of the mouse prostate model
Paul A. Davisa1 c1, Vihas T. Vasua2 p1, Kishorchandra Gohila2, Hyunsook Kima1, Imran H. Khana3, Carroll E. Crossa2 and Wallace Yokoyamaa4
a1 Department of Nutrition, University of California, Davis, CA 95616, USA
a2 Department of Internal Medicine, Division of Pulmonary and Critical Care Medicine, University of California, Davis, CA 95616, USA
a3 Department of Pathology and Laboratory Medicine, Center for Comparative Medicine, University of California, Davis, CA 95616, USA
a4 Processed Foods Research, US Department of Agriculture, Western Regional Research Center, Agricultural Research Service, Albany, CA 94710, USA
Prostate cancer (PCa) has been linked to fat intake, but the effects of both different dietary fat levels and types remain inconsistent and incompletely characterised. The effects on PCa in the transgenic adenocarcinoma of the mouse prostate (TRAMP) cancer model of an elevated fat (20 % of energy as fat) diet containing 155 g of whole walnuts were compared to those of an elevated fat (20 % of energy as soyabean oil) diet with matched macronutrients, tocopherols as well as a low-fat (8 % of energy as soyabean oil) diet. Mice, starting at 8 weeks of age, consumed one of the three different diets ad libitum; and prostates, livers and blood were obtained after 9, 18 or 24 weeks of feeding. No differences were observed in whole animal growth rates in either high-fat (HF) diet group, but prostate tumour weight and growth rate were reduced in the walnut diet group. Walnut diet group prostate weight, plasma insulin-like growth factor 1, resistin and LDL were lower at 18 weeks, while no statistically significant prostate weight differences by diet were seen at 9 or 24 weeks. Multiple metabolites in the livers differed by diet at 9 and 18 weeks. The walnut diet's beneficial effects probably represent the effects of whole walnuts' multiple constituents and not via a specific fatty acid or tocopherols. Moreover, as the two HF diets had dissimilar effects on prostate tumour growth rate and size, and yet had the same total fat and tocopherol composition and content, this suggests that these are not strongly linked to PCa growth.
Source : British Journal of Nutrition
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No Mortality Benefit Seen from PSA Screening.
"Having said that, that's not to say that no man should get PSA testing," he continued. "There are subsets of men in the population at large who do seem to stand a good chance of benefiting from PSA testing.
"Those are men who are young, with no comorbidities, and generally very healthy. These are men with the longest life expectancy overall. They are men who, even if they harbor a nonaggressive, slow-growing cancer, are nonetheless expected to live long enough to die of prostate cancer in the absence of it being identified and treated."
Screening also is reasonable for men who have an above-average risk of prostate cancer, such as African Americans and men with a strong family history of the disease, Andriole added.
The data 0ffered nothing to change the conclusions of an earlier analysis of data from the same study, the National Institutes of Health-sponsored Prostate, Lung, Colorectal, and Ovarian (PLCO) screening program. After a median follow-up of seven years (up to as long as 10 years) the screened and unscreened groups had a similar prostate cancer mortality.
The prostate cancer portion of PLCO involved 76,685 men who were ages 55 to 74 and cancer-free at enrollment. Study participants were randomized to annual PSA screening for six years or to usual care, which sometimes included "opportunistic" PSA screening.
The initial report from the study showed a prostate cancer rate of 116 per 10,000 in the screened group compared with 95 per 10,000 in the control group. Prostate cancer mortality was 2 per 10,000 with screening and 1.7 per 10,000 in the control group.
The current report showed that after a median follow-up of 13 years, cancer incidence was 108.4 and 97.1 per 10,000 in the screened and unscreened groups, respectively. The difference represented a statistically significant 12% increase in cancer incidence in the screened group (RR 1.12, 95% CI 1.07 to 1.17).
Mortality was 3.7 and 3.4 per 10,000 with and without screening, respectively, a nonsignificant difference.
"This article updates with more person-years of follow-up our previously reported finding of no reduction in mortality from prostate cancer in the intervention arm compared with the control arm to 10 years, with no indication of a reduction in prostate cancer mortality to 13 years," the authors wrote of their findings.
Responding to the study, Otis W. Brawley, MD, chief medical officer of the American Cancer Society, acknowledged that the results are consistent with other studies that have pointed to a potential harm from overscreening and unnecessary treatment of indolent prostate cancer.
"This trial does suggest that if there is truly an advantage to mass [PSA] screening it is small," Brawley said in a statement.
Even so, the results do not rule out the possibility of a benefit in some high-risk men or the value of PSA screening in men who want the test, he added.
"I truly believe that a man who is concerned about prostate cancer and understands that experts are not certain that screening saves lives, but it definitely causes anxiety and needless treatment, can reasonably choose to be screened," said Brawley.
Source : MedPage Today
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"A man who is more concerned with unnecessary diagnosis and treatment might reasonably choose not to be screened. It is an area that needs to be left to an informed patient."
Prostate cancer screening with prostate-specific antigen (PSA) afforded no obvious prostate cancer mortality benefit during 13 years of follow-up in a large randomized trial.
In fact, screened patients had a slightly higher prostate cancer mortality: 3.7 per 10,000 person-years, versus 3.4 for unscreened men.
The results emphasize the need to find some means to identify patients who are most likely to benefit from PSA screening, said the first author of a report in the January issue of the Journal of the National Cancer Institute.
"Routine mass screening of the population, purely on the basis of a man's age, is not going to be an effective way of reducing his chance of dying of prostate cancer," Gerald Andriole, MD, of Washington University in St. Louis, told MedPage Today.