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Prostate Cancer

physician assistant

Introduction:

The cause of prostate cancer is unknown, but researchers believe that it results from an acquired or genetic mutation of DNA within prostate cells. According to the American Cancer Society, the lifetime risk of developing prostate cancer is about 15% and the lifetime risk of mortality from prostate cancer is 2.7% (1). Prostate cancer is one of the most common cancers in older men, and is the most frequent cause of cancer related death in men over the age of 75. The probability of developing prostate cancer rises with age. The key to treatment of prostate cancer is the prevention of the disease in the first place. The purpose of Preventive Health Advisor will be to focus on lifestyle habits and Integrative Medicine with potential for prevention of prostate cancer, reduction in risk of prostate cancer, and interventions for those already diagnosed with prostate cancer. These options will include supplements, nutrients, dietary changes, exercise, and screening. Screening is important because symptoms of prostate cancer only occur after it has taken hold, and early detection may have a greater chance of cure. Specific conventional medical and surgical treatment options for prostate cancer will not be discussed here, but guidance of this care will be the responsibility of the patient’s primary care and Urology physicians.

 

Screening for prostate cancer with a digital rectal exam (DRE):

The primary care provider may use this exam to palpate for abnormal nodularity of the prostate gland.

 

Screening for prostate cancer with prostate-specific antigen (PSA) testing:

 

Prostate-specific antigen (PSA) testing after diagnosis of prostate cancer:

PSA testing may be used for guidance of prostate cancer therapy following diagnosis (3).

 

Known risks of prostate cancer:

The various risk factors for prostate cancer include age over 65 years, family history, African American (4), obesity (5), smoking (5), and sedentary lifestyle (5). McGregor SE compared various levels of alcohol intakes and found that prostate cancer risk increased as alcohol consumption increased (6).

 

Prostate cancer and finasteride:

The Prostate Cancer Prevention Trial randomized 18,880 subjects to receive either finasteride or placebo for 7 years and patients were tracked for up to 18 years. In the finasteride group, 10.5% of subjects developed prostate cancer vs. 14.9% in the placebo group. High grade prostate cancer was seen in 3.5% of the finasteride group, and in 3% of the placebo group. Long term survival was similar in both low and high grade prostate cancers compared to their respective placebo groups. Treatment with finasteride resulted in reduction of prostate cancer risk by 30%. (33)

 

Selenium and prostate cancer:

Researchers examined the association between prostate cancer incidence and pre-diagnostic selenium concentrations in toenails. The level of selenium in toenails reflects intake from dietary and supplementary sources. Yoshizawa, et al prospectively examined toenail selenium levels in over 33,000 men, 181 of which later developed advanced prostate cancer (stages C and D) during 2–7 years of follow-up. Results showed the mean toenail selenium level was significantly higher in control subjects than in cancer subjects. It was found that higher selenium levels were associated with a reduced risk of advanced prostate cancer. When subjects in othe highest 20 percent for selenium status were compared with those in the lowest 20 percent, those with the highest selenium status were half as likely to get prostate cancer as those with the lowest levels. The authors reporting an odds ratio (OR) for prostate cancer of 0.4 comparing the highest with the lowest quintile of toenail selenium content. After additionally controlling for family history of prostate cancer, body mass index, calcium intake, lycopene intake, saturated fat intake, vasectomy, and geographical region, the OR was 0.35. According to the authors, these findings suggested that higher selenium intakes may reduce the risk of prostate cancer. (7)

The Nutritional Prevention of Cancer Study Group tested 1312 patients to determine whether or not 200 mcg of selenium would prevent non-melanoma skin cancer in a randomized, double-blind, placebo controlled trial. After this trial, the authors re-evaluated the findings and it was apparent that the prostate cancer risk was much lower in the selenium group. Subjects taking selenium who had the lowest two thirds of serum selenium levels or with a PSA of less than or equal to 4.0 ng/ml at the start of the trial, had a 49% lower incidence of prostate cancer (8,9).

The patients with higher baseline selenium levels at the start of the trial did not benefit from selenium (8,9).

The SELECT trial: Due to prior evidence that selenium and vitamin E may reduce the risk of prostate cancer, the SELECT trial evaluated these two agents for the potential of prostate cancer prevention in a randomized, placebo controlled trial. Over 35,000 men greater than 50 years of age with no sign of prostate cancer by exam or PSA testing were randomized to receive selenium 200 mcg, vitamin E 400 I.U., placebo or both for 7-12 years. Not only did researchers calculate hazard ratios and find that vitamin E significantly increased the risk of prostate cancer compared with placebo, they also determined that prostate cancer was not prevented by selenium supplementation. (10,11)

A case cohort study by Kristal AR, et al looked at the baseline selenium status of patients from the SELECT trial who developed prostate cancer and were matched to a cohort of 3117 men without prostate cancer. The men in the trial took 200 mcg of selenium and 400 I.U. of vitamin E. Out of 1739 cases of prostate cancer, 489 cases of prostate cancer were aggressive forms of the disease with poor prognosis. Selenium status was determined by using the toenails of men sent for analysis. The authors found that (12):

Also, please see the selenium section in Preventive Health Advisor to research benefits of selenium intake and foods high in selenium.

 

Flaxseed supplementation and prostate cancer:

A pilot study in prostate cancer patients suggests that a low-fat, flaxseed-supplemented diet decreases prostate-specific antigen (PSA) and cholesterol levels as well as benign prostatic epithelial cell proliferation. Fifteen men who were scheduled to undergo repeat prostate biopsy were instructed to follow a low-fat (less than 20% kcal), flaxseed-supplemented (30 g/day) diet for 6-months. At the end of the study period, significant decreases in PSA (8.47 to 5.72 ng/mL; P = 0.0002) and cholesterol (241.1 to 213.3 mg/dL; P = 0.012) were seen. Significant change was not observed in total testosterone. A significant decrease in proliferation rates in the benign epithelium from 0.022 to 0.007 (P = 0.0168) was observed. (13)

A total of 161 men diagnosed with prostate cancer and scheduled at least 21 days before prostatectomy were randomized into 4 groups – control (usual diet), flaxseed-supplemented (30gm/day), low-fat diet (<20% of energy from dietary fat), or flaxseed-supplemented plus low fat. Dietary questionnaires, serum and urine levels of relevant compounds and prostatectomy tissue were assessed. The primary study endpoint was proliferation index (by Ki-67 staining using the antibody MIB-1) in the prostatectomy tissue. Men were on treatment for an average of 30 days. Tumor proliferation was significantly lower in the flaxseed-supplemented arm (proliferation index = 1.66), compared to 3.23 for controls, 2.56 for low-fat diet, and 1.50 for the combined flaxseed with low-fat diet. No differences were noted between groups for apoptosis (programmed cell death) and most serologic (identification of antibodies in the blood serum) endpoints. Men in the low-fat diet group had significant reductions in body mass index and total and low-density lipoprotein cholesterol (p= 0.048). Findings suggest that flaxseed may be protective for prostate cancer and provides evidence for low-fat diets to manage cholesterol. (14)

 

Lycopene and prostate cancer:

Lycopene is the pigment responsible for the red in color of tomatoes. Lycopene consumed in the diet or used as a supplement is controversial in its use for the prevention of prostate cancer. The most recent study included below supports lycopene as having good potential in prevention of prostate cancer which did not relay any evidence of significant harm of this nutrient.

During the Prostate Cancer Prevention Trial, lycopene levels were obtained at the same time that finasteride was studied for potential of prostate cancer chemoprevention over the course of 7 years. There was no correlation found between serum lycopene levels and the risk of prostate cancer. (15)

Researchers performed a systematic review using 8 randomized controlled trials with lycopene to determine whether or not it may prevent either benign prostatic hypertrophy (BPH) or prostate cancer. It was determined by the authors that there was a variable degree of quality in the design of the studies and that evidence was not strong enough to support the use of lycopene for prevention of BPH or prostate cancer. (16)

A prospective study interpreted data from 49,898 men ages 40-75 who were part of the Health Professionals Follow-Up Study. The subjects answered questions at regular intervals about lifestyle and dietary habits from 1986 until and including 2010. The men who consumed more lycopene, lower amounts of alcohol, lower fat intake, less coffee, but more fruit, vegetables, and fiber were found to have a 28% lower risk of all types of prostate cancer and a 53% lower risk of dying from prostate cancer determined by hazard ratios. The study compared the highest quintile of lycopene intake (about 13,400 mcg per day) with the lowest quintile of lycopene intake (about 3200 mcg per day) in men who had one or more negative PSA testing result. Higher angiogenesis is associated with more aggressive tumors. Men diagnosed with prostate cancer who previously provided fixed tumor tissue showed that the highest quintile of lycopene intake had biomarkers in the tumors suggestive of less angiogenesis. Researchers also determined that men who consumed a higher lycopene intake in the early phase of the study had a lower risk of prostate cancer than those with lycopene intake later in the study. (17)

 

Excess calcium intake appears to increase the risk of prostate cancer:

A study which evaluated a cohort of over 65,000 men over a period of 6-7 years revealed that intake of calcium over 2000 mg per day in the form of dietary and supplement intake was associated with a moderate increase in risk of prostate cancer. The risk of prostate cancer was not increased with dairy intake. There was also no increase in risk of prostate cancer with moderate or low levels of dietary calcium intake. (31)

Chung et al reviewed calcium and prostate cancer risk as part of a systematic review of health outcomes. He found that a number of studies reported that high calcium intakes were associated with an increased risk of prostate cancer. (32)

 

Prostate cancer and ginger extract:

Ginger extract, previously shown to display anti-inflammatory, antioxidant and anti-proliferative activities, might be useful for prostate cancer. Feeding mice 100 mg/kg of ginger extract/day inhibited growth of prostate cancer xenografts (the transmission of living organs, tissues, or cells from one species to another) in nude mice by approximately 56%, as shown by measurements of tumor volume. This finding suggests that whole ginger extract has promising cancer-preventing activity in prostate cancer by stopping the growth of cancer cells, as well as in inducing cell death in prostate cancer cells. Of great importance was that the extract did not show significant toxicity to normal tissues, such as bone marrow. (18)

 

Prostate cancer and dietary modifications:

Epidemiologic studies:

After reviewing 46 published research studies, Gathirua-Mwangi and Zhang reported an increase in risk of advanced prostate cancer in those with a regular dietary intake of thoroughly cooked meats, saturated fat, and calcium (19).

 

Mediterranean diet and prostate cancer:

A literature review study by Ferrís-Tortajada, J et al expressed that the risk of prostate cancer is reduced on those with intake of a Mediterranean diet when compared to a Western-style diet with foods high in meat and saturated fat (20).

A Mediterranean style diet generally consisted of a variety of fruits, vegetables, whole grains, olive oil, legumes, nuts, beans, herbs, seeds, and spices as the primary basis for each meal. Fish and seafood is eaten often at least twice per week. Yogurt, poultry, eggs, and cheese is consumed in moderate portions daily to weekly. Meats and sweets are eaten infrequently. (21)

 

Fish intake and prostate cancer:

A cohort study from Japan reviewed data from 5589 men age 30-79 and found that those men who consumed a higher intake of fish had a lower risk of dying from prostate cancer than those with a lower intake of fish (30). A review and meta-analysis confirmed that prostate cancer mortality was lower among subjects with fish consumption, but there was no reduction seen in the incidence of prostate cancer (22).

 

Fiber intake and prostate cancer:

Deschasaux, M et al followed 3313 men over the course of 12 years. The authors calculated the risk of prostate cancer using hazard ratios and found the following conclusions. The groups with the highest total fiber, highest insoluble fiber, and highest legume intake had a 53%, 54%, and 45% lower risk of prostate cancer respectively when compared to the lowest intakes. In this study, soluble fiber, vegetable, and fruit intake did not lower or increase the risk of prostate cancer. (23)

 

Prostate cancer and vegetables:

Cohen, JH et al compared fruit and vegetable intakes in a group of 628 men under 65 years old recently diagnosed with prostate cancer with a matched cohort . The study used questionaires to track dietary habits of the men over 3 to 5 years and compared their dietary intakes. The authors noted the following findings (24):

 

Prostate cancer and allium vegetables:

A population-based, case–control study performed on 238 patients with prostate cancer and 471 male control subjects in China investigated the association between intake of allium vegetables including garlic, scallions, onions, chives, and leeks, and the risk of prostate cancer. It was found that men in the category of highest intake of allium vegetables (>10 grams daily) had a 49% risk reduction of contracting prostate cancer than did those in the category of lowest intake (2.2 grams daily).  Reductions in risk for men in the highest intake categories (compared to the lowest intake categories) for garlic was 53% (OR = 0.47) and 70% for scallions consumption (OR = 0.30). These benefits were more significant in men with localized, rather than advanced prostate cancer and were independent of body size, intake of other foods and total calorie intake. These results suggested that the allium group of vegetables have cancer preventative properties and it may be worthwhile for patients to increase their intake of these vegetables. (25)

 

Dairy products, calcium, vitamin D and prostate cancer:

Consumption of dairy products, calcium, and vitamin D showed no increase in the risk of prostate cancer in a review and meta-analysis of 45 observational studies. Cohort studies demonstrated no link between dairy or milk consumption and increased risk of prostate cancer nor did case control studies of calcium intake. Additionally, dietary intake of vitamin D was not correlated with increased prostate cancer risk. (26)

 

Prostate cancer and exercise:

Epidemiological evidence for prostate cancer prevention: Heitkamp and Jelas evaluated past and current epidemiological evidence for the prevention of prostate cancer with exercise. 32 case control studies and 17 case control studies were reviewed by the authors. The authors concluded that exercise done for recreation or employment related purposes did not appear to reduce the risk of prostate cancer. However, the studies which included intense exercise programs have shown to represent good evidence for prostate cancer prevention. (27)

Factors of race and exercise on prostate cancer risk: Different activities may be measured in terms of MET hours, (Metabolic Equivalent Task) hours, which is a unit used to describe energy expended in a physicial activity. For instance, a slow walk is about 2 METs, walking fast is about 4 METs, jogging at a 12 minute mile is about 8 METs, and running a 10 minute mile is about 10 METs. A prospective study followed exercise habits of 164 white men and 143 black men planned for prostate biopsy. The white men who exercised 9 or more MET hours per week were 53% less likely to have a biopsy positive for prostate cancer than white men who exercised under 9 MET hours per week (odds ratio of 0.47). The risk of having a positive biopsy result was not reduced in black men who exercised, and according to the authors, more research is needed on why exercise did not improve risk in black men. (4)

 

Effects of exercise on prostate tumor cells:

Barnard, et al. used the blood from 3 different groups of 51 to 64 year old males to treat cultured prostate cancer cells in the lab. They used an exercise group that did a consistent exercise program for at least 10 years, a diet plus exercise group who did a consistent diet and exercise program for at least 10 years, and a placebo group. The diet and exercise group were part of a “Pritikin” program and ate low fat, high fiber and complex carbohydrates along with exercise 4-6 days per week. The exercise group exercised for 1 hour per day 5 days per week at a University program in Nevada but did not have any diet program. The placebo subjects were sedentary with poor dietary intake and felt to be at risk of prostate cancer. Blood was taken from the subjects and placed onto prostate cancer cells in vitro. The blood from the diet plus exercise group caused a significantly greater rate of apoptosis and lower growth rate in of the prostate cancer cells than the exercise alone or placebo groups. (28)

Rundqvist, H et al also found that serum samples after exercise inhibited growth of tumor cells (29).

 

 

Assessment and Plan: Prostate Cancer

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

References:

1.American Cancer Society. Lifetime Risk of Developing or Dying From Cancer. Accessed 3/1/2014. http://www.cancer.org/cancer/cancerbasics/lifetime-probability-of-developing-or-dying-from-cancer

 

2.Vickers AJ, Lilja H. Predicting prostate cancer many years before diagnosis: how and why? World J Urol. 2012 Apr;30(2):131-5. http://www.ncbi.nlm.nih.gov/pubmed/22101902

 

3.Peter Carroll, MD, Chair; Peter C. Albertsen, MD, Vice Chair; Kirsten Greene, MD, Facilitator; Richard J. Babaian, MD; H. Ballentine Carter, MD; Pater H. Gann, MD, ScD; Misop Han, MD; Deborah Ann Kuban, MD; A. Oliver Sartor, MD; Janet L. Stanford, MPH, PhD; Anthony Zietman, MD. PSA Testing for the Pretreatment Staging and Posttreatment Management of Prostate Cancer: 2013 Revision of 2009 Best Practice Statement Panel Members: American Urologic Association, 2013. http://www.auanet.org/common/pdf/education/clinical-guidance/Prostate-Specific-Antigen.pdf

 

4.Singh AA, Jones LW, Antonelli JA, Gerber L, Calloway EE, Shuler KH, Freedland SJ, Grant DJ, Hoyo C, Bañez LL. Association between exercise and primary incidence of prostate cancer: does race matter? Cancer. 2013 Apr 1;119(7):1338-43. http://www.ncbi.nlm.nih.gov/pubmed/23401030

 

5.Chan JM, Van Blarigan EL, Kenfield SA. [Epub ahead of print]What should we tell prostate cancer patients about (secondary) prevention? Curr Opin Urol. 2014 Mar 12. http://www.ncbi.nlm.nih.gov/pubmed/24625429

 

6.McGregor SE, Courneya KS, Kopciuk KA, Tosevski C, Friedenreich CM. Case-control study of lifetime alcohol intake and prostate cancer risk.Cancer Causes Control. 2013 Mar;24(3):451-61. http://www.ncbi.nlm.nih.gov/pubmed/23271409

 

7.Yoshizawa K, Willett WC, Morris SJ, Stampfer MJ, Spiegelman D, Rimm EB, Giovannucci E. Study of prediagnostic selenium level in toenails and the risk of advanced prostate cancer. J Natl Cancer Inst. 1998 Aug 19;90(16):1219-24. http://www.ncbi.nlm.nih.gov/pubmed?term=9719083

 

8.Clark LC, Combs GF Jr, Turnbull BW, et al.: Effects of selenium supplementation for cancer prevention in patients with carcinoma of the skin. A randomized controlled trial. Nutritional Prevention of Cancer Study Group. JAMA 276 (24): 1957-63, 1996. http://www.ncbi.nlm.nih.gov/pubmed/8971064

 

9.Duffield-Lillico AJ, Dalkin BL, Reid ME, Turnbull BW, Slate EH, Jacobs ET, Marshall JR, Clark LC; Nutritional Prevention of Cancer Study Group. Selenium supplementation, baseline plasma selenium status and incidence of prostate cancer: an analysis of the complete treatment period of the Nutritional Prevention of Cancer Trial. BJU Int. 2003 May;91(7):608-12. http://www.ncbi.nlm.nih.gov/pubmed/12699469

 

10.Lippman SM, Klein EA, Goodman PJ, Lucia MS, Thompson IM, Ford LG, Parnes HL, Minasian LM, Gaziano JM, Hartline JA, Parsons JK, Bearden JD 3rd, Crawford ED, Goodman GE, Claudio J, Winquist E, Cook ED, Karp DD, Walther P, Lieber MM, Kristal AR, Darke AK, Arnold KB, Ganz PA, Santella RM, Albanes D, Taylor PR, Probstfield JL, Jagpal TJ, Crowley JJ, Meyskens FL Jr, Baker LH, Coltman CA Jr. Effect of selenium and vitamin E on risk of prostate cancer and other cancers: the Selenium and Vitamin E Cancer Prevention Trial (SELECT). JAMA. 2009 Jan 7;301(1):39-51. http://www.ncbi.nlm.nih.gov/pubmed/19066370

 

11.Klein EA, Thompson IM Jr, Tangen CM, Crowley JJ, Lucia MS, Goodman PJ, Minasian LM, Ford LG, Parnes HL, Gaziano JM, Karp DD, Lieber MM, Walther PJ, Klotz L, Parsons JK, Chin JL, Darke AK, Lippman SM, Goodman GE, Meyskens FL Jr, Baker LH. Vitamin E and the risk of prostate cancer: the Selenium and Vitamin E Cancer Prevention Trial (SELECT). JAMA. 2011 Oct 12;306(14):1549-56. http://www.ncbi.nlm.nih.gov/pubmed/21990298

 

12.Kristal AR, Darke AK, Morris JS, Tangen CM, Goodman PJ, Thompson IM, Meyskens FL Jr, Goodman GE, Minasian LM, Parnes HL, Lippman SM, Klein EA. [Epub ahead of print] Baseline Selenium Status and Effects of Selenium and Vitamin E Supplementation on Prostate Cancer Risk. J Natl Cancer Inst. 2014 Feb 22.  http://www.ncbi.nlm.nih.gov/pubmed/24563519

 

13.Demark-Wahnefried W, Robertson CN, Walther PJ, Polascik TJ, Paulson DF, Vollmer RT. Pilot study to explore effects of low-fat, flaxseed-supplemented diet on proliferation of benign prostatic epithelium and prostate-specific antigen. Urology. 2004 May;63(5):900-4. http://www.ncbi.nlm.nih.gov/pubmed/15134976

 

14.Demark-Wahnefried W, Polascik TJ, George SL, Switzer BR, Madden JF, Ruffin MT 4th, Snyder DC, Owzar K, Hars V, Albala DM, Walther PJ, Robertson CN, Moul JW, Dunn BK, Brenner D, Minasian L, Stella P, Vollmer RT. Flaxseed supplementation (not dietary fat restriction) reduces prostate cancer proliferation rates in men presurgery. Cancer Epidemiol Biomarkers Prev. 2008 Dec;17(12):3577-87. http://www.ncbi.nlm.nih.gov/pubmed/19064574

 

15.Kristal AR, Till C, Platz EA, Song X, King IB, Neuhouser ML, Ambrosone CB, Thompson IM.

Serum lycopene concentration and prostate cancer risk: results from the Prostate Cancer Prevention Trial.

Cancer Epidemiol Biomarkers Prev. 2011 Apr;20(4):638-46. http://www.ncbi.nlm.nih.gov/pubmed/21335507

 

16.Ilic D, Misso M. Maturitas. Lycopene for the prevention and treatment of benign prostatic hyperplasia and prostate cancer: a systematic review. 2012 Aug;72(4):269-76. http://www.ncbi.nlm.nih.gov/pubmed/22633187

 

17.Zu K, Mucci L, Rosner BA, Clinton SK, Loda M, Stampfer MJ, Giovannucci E. Dietary lycopene, angiogenesis, and prostate cancer: a prospective study in the prostate-specific antigen era. J Natl Cancer Inst. 2014 Feb;106(2):djt430. http://www.ncbi.nlm.nih.gov/pubmed/24463248

 

18.Karna P, Chagani S, Gundala SR, Rida PC, Asif G, Sharma V, Gupta MV, Aneja R. Benefits of whole ginger extract in prostate cancer. Br J Nutr. 2012 Feb;107(4):473-84. http://www.ncbi.nlm.nih.gov/pubmed/21849094

 

19.Gathirua-Mwangi WG, Zhang J. Dietary factors and risk for advanced prostate cancer. Eur J Cancer Prev. 2014 Mar;23(2):96-109. http://www.ncbi.nlm.nih.gov/pubmed/23872953

 

20.Ferrís-Tortajada J, Berbel-Tornero O, García-Castell J, Ortega-García JA, López-Andreu JA. [Dietetic factors associated with prostate cancer: protective effects of Mediterranean diet]. [Article in Spanish] Actas Urol Esp. 2012 Apr;36(4):239-45. http://www.ncbi.nlm.nih.gov/pubmed/21959061

 

21.Mayo Clinic. Mediterranean diet: A heart-healthy eating plan. Website accessed 02/07/2014. http://www.mayoclinic.org/mediterranean-diet/art-20047801

 

22.Szymanski KM, Wheeler DC, Mucci LA. Fish consumption and prostate cancer risk: a review and meta-analysis. Am J Clin Nutr. 2010 Nov;92(5):1223-33. http://www.ncbi.nlm.nih.gov/pubmed/20844069

 

23.Deschasaux M1, Pouchieu C, His M, Hercberg S, Latino-Martel P, Touvier M. Dietary Total and Insoluble Fiber Intakes Are Inversely Associated with Prostate Cancer Risk. J Nutr. 2014 Feb 19. [Epub ahead of print]. http://www.ncbi.nlm.nih.gov/pubmed/24553693

 

24.Cohen JH, Kristal AR, Stanford JL. Fruit and vegetable intakes and prostate cancer risk. J Natl Cancer Inst. 2000 Jan 5;92(1):61-8. http://www.ncbi.nlm.nih.gov/pubmed/10620635

 

25.Hsing AW, Chokkalingam AP, Gao YT, Madigan MP, Deng J, Gridley G, Fraumeni JF Jr. Allium vegetables and risk of prostate cancer: a population-based study. J Natl Cancer Inst. 2002 Nov 6;94(21):1648-51. http://www.ncbi.nlm.nih.gov/pubmed/12419792

 

26.Huncharek M, Muscat J, Kupelnick B. Dairy products, dietary calcium and vitamin D intake as risk factors for prostate cancer: a meta-analysis of 26,769 cases from 45 observational studies. Nutr Cancer 2008;60(4):421-41. http://www.ncbi.nlm.nih.gov/pubmed/18584476

 

27.Heitkamp HC, Jelas I. Epidemiological evidence for preventing prostate cancer by physical activity. [Article in German] Wien Med Wochenschr. 2012 Dec;162(23-24):533-40. http://www.ncbi.nlm.nih.gov/pubmed/23065019

 

28.Barnard , James R., Tung H. Ngo, Pak-Shan Leung, William J. Aronson, and Lawrence A. Golding. A Low-Fat Diet and/or Strenuous Exercise Alters the IGF Axis In Vivo and Reduces Prostate Tumor Cell Growth In Vitro. The Prostate 56:201-206 May 2003. http://www.ncbi.nlm.nih.gov/pubmed/12772189

 

29.Rundqvist H, Augsten M, Strömberg A, Rullman E, Mijwel S, Kharaziha P, Panaretakis T, Gustafsson T, Östman A. Effect of acute exercise on prostate cancer cell growth. PLoS One. 2013 Jul 5;8(7):e67579. http://www.ncbi.nlm.nih.gov/pubmed/23861774

 

30.Pham TM, Fujino Y, Kubo T, Ide R, Tokui N, Mizoue T, Ogimoto I, Matsuda S, Yoshimura T. Fish intake and the risk of fatal prostate cancer: findings from a cohort study in Japan. Public Health Nutr. 2009 May;12(5):609-13.  http://www.ncbi.nlm.nih.gov/pubmed/18664313

 

31.Rodriguez C, McCullough ML, Mondul AM, Jacobs EJ, Fakhrabadi-Shokoohi D, Giovannucci EL, Thun MJ, Calle EE. Calcium, dairy products, and risk of prostate cancer in a prospective cohort of United States men. Cancer Epidemiol Biomarkers Prev. 2003 Jul;12(7):597-603. http://www.ncbi.nlm.nih.gov/pubmed/12869397

 

32.Chung M, Balk EM, Brendel M, Ip S, Lau J, Lee J, Lichtenstein A, Patel K, Raman G, Tatsioni A, Terasawa T, Trikalinos TA. Vitamin D and calcium: a systematic review of health outcomes. Evid Rep Technol Assess (Full Rep). 2009 Aug;(183):1-420. http://www.ncbi.nlm.nih.gov/pubmed/20629479

 

33.Thompson IM Jr, Goodman PJ, Tangen CM, Parnes HL, Minasian LM, Godley PA, Lucia MS, Ford LG. Long-term survival of participants in the prostate cancer prevention trial. N Engl J Med. 2013 Aug 15;369(7):603-10. http://www.ncbi.nlm.nih.gov/pubmed/23944298

 

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