Research Paper

Modifiable risk factors of prostate cancer: Insights from a hospital-based study

Copyright: © 2026 Kulshekar et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

ABSTRACT

Introduction: Prostate Cancer (PCa) is the second most common cancer and the fifth leading cause of cancer among men worldwide. The prevalence of Prostate cancer is much lower in India and it is likely that the incidence of prostate cancer will show an increase in the future. Modifiable habits like smoking, tobacco chewing, alcohol consumption and others have shown to be associated with Prostate Cancer. All these variables show conflicting results in various studies. Hence more research on the various determinants of Prostate Cancer for the Indian population will help in reducing the burden of this disease through scientific and empirical approach. The present study aims to study association of various modifiable risk factors with Prostate Cancer and Benign Prostatic Hyperplasia.

Methods: 72 histologically proven prostate ‘Cancer Cases’ and 132 ‘BPH controls’ were included for the study after obtaining their Informed Consent. This was confirmed by performing the PSA (Prostate Specific Antigen Test), DRE (Digital Rectal Examination) test and histopathological investigations. Odds ratio was obtained to study the association of the risk factors.

Results: Our study revealed that Modifiable risk factors associated with decreased risk of Prostate cancer are Coffee intake and meat with an odds ratio of 0.355 (95% CI 0.175 to 0.72, p = 0.004) and 0.516 (95% CI 0.269 to 0.992, p = 0.047). No significant association was observed with other modifiable risk factors.

Conclusions: The present study concludes that an increased intake of coffee and meat may be linked to a reduced risk of developing prostate cancer.

INTRODUCTION

The second most frequent type of cancer in males and the fifth largest cause of cancer-related deaths globally is Prostate Cancer (PCa) [1, 2]. Although the Prostate Cancer incidence in Indians is lower when compared to the Western population, it is expected that the number of PCa cases shall increase in the years to come [3, 4]. As per the Indian Cancer Registry 2020 data, PCa accounted for 3% of all cancers in India with close to 40,000 cases being reported annually and an increase in 30% of cases in the last 25 years. The data on the modifiable lifestyle risk factor of prostate cancer is limited for any population and debatable. Many studies have shown alcohol, smoking, tea, coffee, red meat and occupational hazards as associated risk factors for PCa [5–8]. There are fewer studies reported on the Prostate Cancer modifiable risk factors for the Indian population. The present study will summarize the association of these risk factors and their potential mechanisms involved in development or prevention.

RESULTS

The participant’s demographics and distribution of habits are summarized in Table 1 and Table 2. The mean age was 72 (±9.2) years for cases and 65 (±8.46) years for controls. Study participants were majorly in the age group between 61–80 years (74%). Among the cases, there was an overwhelming majority (86%) of the participants from rural areas when compared to the urban population. (Table 1). Multivariate logistic regression analysis was performed to evaluate the association between variables and outcome. (Table 3). In the unadjusted analysis, tobacco use (OR = 2.63, 95% CI: 1.41–4.91, p = 0.002) and smoking (OR = 2.54, 95% CI: 1.38–4.66, p = 0.003) were significantly associated with higher odds of the outcome. Coffee intake (OR = 0.30, 95% CI: 0.15–0.58, p = 0.001) and meat consumption (OR = 0.40, 95% CI: 0.22–0.74, p = 0.003) were associated with significantly lower odds of the outcome. After adjusting for covariates, the associations for tobacco and smoking were attenuated and became statistically non-significant. However, coffee consumption remained strongly protective (adjusted OR = 0.36, 95% CI: 0.18–0.72, p = 0.004), and meat consumption also retained a protective effect with borderline significance (adjusted OR = 0.52, 95% CI: 0.27–0.99, p = 0.047). Farming occupation showed no significant association with the outcome in either unadjusted or adjusted models. Very small numbers in the contingency table, led to infinite or undefined Odds Ratio value for Tea (Table 3).

Molecular mechanism in carcinogenesis

Alcohol consumption causes Prostate carcinogenesis by several mechanisms however, metabolites of ethanol such as acetaldehyde are significant in driving the growth of cancer cells and raising the metastatic potential of tumours [6, 9]. The protective function of nutrients such as trans-vaccenic acid found in meat improves immune response to cancer [10]. On the other hand, red meat contains recognized carcinogens, such as polycyclic aromatic hydrocarbons (PAHs) and heterocyclic amines (HCAs) [11, 12].

Several studies suggest that the main antioxidants found in green tea referred to as catechins, (-)epigallocatechin-3-gallate (EGCG), (-)-epigallocatechin (EGC) are known to inhibit tumorigenesis and tumour progression, [13]. Other polyphenols such as Flavonoids have been shown to increase the mRNA expression of tumor suppressor genes, thereby suppressing carcinogenesis [14, 15]. Cafestol and Kahweol present in coffee have anti-cancer properties [16]. Coffee contains antioxidant compounds such as caffeine, phenolic compounds and melanoidins which show protective function [17]. In addition, they also exhibit other important mechanisms such as anti-inflammatory, DNA damage control, and transcriptional factors modulation which prevent tumour growth [18]. One of the major causes of various types of cancers is Smoking. The molecular mechanisms state that the mutation by tobacco-related carcinogens may cause mutations of cancer progression genes [19]. Other hypotheses involve hormone alterations, the proliferation of tumour angiogenesis, and immune suppression [20]. According to recent research, neutrophil extracellular traps, or NETs, may have a role in a number of pathophysiological diseases, including cancer [21]. It has been discovered that smoking cigarettes causes vascular injury in a number of organs, including prostate cancer, through endothelial damage, oxidative stress, chronic inflammation, and local hypoxia [22]. Smokeless tobacco -products undergo fermentation which produces nitrosamines, the potential carcinogens [23]. Other possible mechanisms include exposure to aldehydes and metals, which have been associated with inflammation and increased cell proliferation [24]. Tobacco chewing also enhances the levels of ROS and increases the expression of inflammatory markers such as IL-18 which has an important role to play in tumourogenesis. It is also known to diminish the DNA repair mechanism [25]. Several organophosphate insecticides cause aggressive forms of cancer due to their role in the progression of cancer rather than initiation [26]. Organochlorine pesticides are endocrine disruptors that trigger PCa development [27, 28]. In addition to specific pesticides, a farmer may be exposed to several other chemicals such as mononuclear aromatic hydrocarbons, polycyclic aromatic hydrocarbons from petroleum, gasoline engine emissions, acetic acid arsenic compounds, lubricating oils and greases, diesel engine emission and alkanes whose role need to be investigated [29].

DISCUSSION

Modifiable Risk factors for prostate cancer have been well identified and supported by strong data. Some of these include the consumption of alcohol, tea, coffee, meat, smoking, tobacco chewing, and heavy physical activities such as farming have been discussed below. Of all the seven risk factors studied here, only coffee and meat consumption showed a significant association as depicted in Figure 1.

Alcohol

The present study does not show an association between PCa and alcohol. This finding is comparable to another case-control study which was conducted by Ganesh et al. [5] however contradicts a study conducted in Delhi [30, 31]. Results from other studies have shown that with the increase in the number of doses, the risk of prostate cancer increases considerably [32]. A meta-analysis report suggested that alcohol consumption does increase the risk of morbidity and mortality [33]. A study conducted by Vartolomei et al. presented that PCa risk increases even with the consumption of white wine when compared to red wine [34]. However, among healthy subjects, a correlation was found between heavy alcohol use and a higher risk of dying from prostate cancer [35].

Meat

In this study, meat consumption did show a significant association with PCa. This is supported by a similar study which stated that higher intakes of poultry 60 g/d and 30 g/d when substituted with red meat or unprocessed meat was linked to a noticeably lower incidence of recurrence [36].A meta-analysis of the Asian population concluded that there is no association between prostate cancer risk and poultry consumption [37]. This is similar to a prospective meta-analysis which suggested that the consumption of red meat is not linked to prostate cancer [38]. Earlier studies do conclude that less meat consumption does not lower the chance of developing prostate cancer [39]. Contrary, an organized analysis study does indicate that higher prostate cancer risk is associated with “total meat” consumption [40].Studies do suggest that replacing red meat with leaner proteins such as skinless poultry should be the diet of choice [41]. Studies have also concluded that a “plant source” diet unlike meat is protective against Prostate Cancer [42]. Our study restricted data collection to total meat consumption and not the kind of meat which should be taken up in future studies considering its significant association.

Tea

Our research indicates no correlation between tea drinking and the incidence of prostate cancer. On the contrary, tea consumption in US states reduces the risk of PCa [43]. Our study also contradicts other studies which show an association between an increase in consumption of tea and a lower risk of Prostate cancer [44]. According to a meta-analysis, tea consumption could not bring a reduction in cancer and has additionally been demonstrated to raise the risk of prostate cancer [45, 46]. Further, the association of other types such as Green Tea is also not explored in our study which is shown to be protective in some studies [47, 48]. Being one of the common beverages consumed in India, the understanding between Tea consumption and its association with the development of cancer has always been unclear. From historical times, the consumption of tea is considered to be beneficial and preventive to the development of many diseases including Cancer. However, no clear statistical data is available [49].

Coffee

Our study showed a 65% less chance of developing PCa with the intake of Coffee. A systematic review and meta-analysis on the intake of Coffee and PCa for a very large cohort has indicated that prostate cancer risk is lowered with increased intake of coffee [50, 51]. It is also comparable with another study which concludes that six or more cups of coffee per day, less the risk for lethal PCa [52]. A study conducted in the UK concluded that aggressive PCa risk is lowered with coffee consumption but not its overall risk [53]. Another meta-analysis for both cohort and casecontrol studies revealed that an increase in coffee intake may or may not decrease the risk of prostate cancer [54]. Our current study showed a significant association between the two. Hence, may be considered as a health recommendation to prevent the disease.

Smoking

No positive association between smoking and PCa incidence was observed in a large cohort meta-analysis study [55]. This is comparable to another similar study which concludes that there is a lower risk of prostate cancer in smokers [56]. A study by Lora et al. indicated that smoking may be moderately associated with an increased risk of PCa [57]. This is contradictory to another study that reveals smoking has a lower risk for PCa [58]. Mortality and aggressive PCa forms also show an association with smoking in some studies [59]. Smoking is an established causative agent for cancer mortality in India, despite that our present study shows no association between smokers amongst prostate cancer. Our study also did not consider the kind of smoking or doseresponse and prostate cancer incidence, which may be intervened in the future, studies.

Tobacco chewing

In rural India close to 40% of cancer patients still consume tobacco leaves and other tobacco products [60]. About 28 known carcinogens have been identified in smokeless tobacco [61].

Several prospective and retrospective studies have implicated the role of smokeless tobacco and the development of various cancers [62–64]. Tobacco chewing is one of the most common practices in this part of the country. Globally, India ranks third in production of tobacco and consumes 50% of it [65]. Numerous research studies have linked tobacco and its product use to a variety of deadly malignancies. However, our study has found to have no possible association between chewing and prostate cancer.

Farming

A wide array of activities are involved in farming that enhance the exposure to potentially diverse agents such as pesticides, and insecticides that increase the risk of PCa [29, 66, 67]. Several Case-control and mortality studies are comparable with each other concerning their positive association with prostate cancer [68–70]. In another study by Meyer et al. on Caucasians, exposure to various farming activities showed an association with an increased risk of prostate cancer [71]. This finding is similar to the study conducted by Krstev et al. [72]. The use of pesticides in farming is one of the most common occupational hazards responsible for prostate carcinogenesis [71]. Our study did not show any association and does not have information on the kind of farming practices and type of chemicals the farmers are exposed to which can be evaluated in future studies.

MATERIALS AND METHODS

Study population

The present observational cross-sectional study was conducted at a tertiary care hospital in the city of Belagavi between 2020 and 2022. The data was analysed thereafter. An approval from the institutional ethics committee was secured and a total of 72 Prostate Malignancy cases (outcome of interest) and 132 Benign Prostatic Hyperplasia cases (controls) were included in our study.

The association of seven modifiable lifestyle risk factors was studied in each group.

Data collection and statistical evaluation

All patients admitted to the Department of Urology as confirmed cases of Prostate Cancer and BPH were included in the study. After obtaining the Informed Consent of the patients, they filled out the questionnaire. All questions included in the questionnaire were single-choice questions. Data was entered into the SPSS software (version 20.0). Multivariate Logistic Regression analysis was completed to understand the association and odds ratios were estimated.

CONCLUSIONS

The current study concludes that meat and coffee are the protective factors. Hence more studies must be taken up to understand the underlying mechanism and bioactive compounds present in them. In this study, most of the cases were from rural areas unlike what has been reported in cancer registries which were based on urban population. Although no association was seen between PCa, smoking and alcohol consumption. The data obtained here may not be relevant due to social discrimination and stigma involved with the perception of these two risk factors. The primary objective of the study was to assess overall consumption frequency rather than detailed dietary characterization which is not addressed here. Our study does have major limitations such as a being a hospital based study which limits the generalizability of results to broader community setting. Results from individuals who seek hospital care such as BPH and Prostate Cancer patients may vary systematically from the general population. Other limitations include recall bias, smaller sample size, inclusion of a few risk factors, non-inclusion of dietary dose-response, and exposure time of the risk factors which may be overcome by prospective preclinical studies and animal model studies. Future studies incorporating local consumption patterns in larger, multicenter prospective cohorts may be taken up to confirm associations. Developing countries like India have medical resources and hence can formulate strategies that prevent the disease by creating awareness among the population.

AUTHOR CONTRIBUTIONS

MK: Data Collection, analysis and manuscript writing. AP and RN: Manuscript revision and critical edits.

ACKNOWLEDGMENTS

We sincerely thank the nursing staff for their invaluable support in helping patients provide more accurate responses during data collection.

CONFLICTS OF INTEREST

Authors have no conflicts of interest to declare.

ETHICAL STATEMENT

This study was conducted in accordance with the ethical standards. Ethical approval for this study was obtained from the KAHER Ethics Committee on Human Subjects (Approval number: KAHER/EC/19-20/290619009).

CONSENT

Informed consent was obtained from all individual participants included in the study. Participants were informed about the purpose of the study, their right to withdraw at any time, and the measures taken to ensure confidentiality.

FUNDING

No funding was used for this paper.

• 1 Bergengren O, Pekala KR, Matsoukas K, Fainberg J, Mungovan SF, Bratt O, Bray F, Brawley O, Luckenbaugh AN, Mucci L, Morgan TM, Carlsson SV. 2022 Update on Prostate Cancer Epidemiology and Risk Factors-A Systematic Review. Eur Urol. 2023; 84:191–206. https://doi.org/10.1016/j.eururo.2023.04.021 PMID:37202314
• 2 Rawla P. Epidemiology of Prostate Cancer. World J Oncol. 2019; 10:63–89. https://doi.org/10.14740/wjon1191 PMID:31068988
• 3 Hariharan K, Padmanabha V. Demography and disease characteristics of prostate cancer in India. Indian J Urol. 2016; 32:103–8. https://doi.org/10.4103/0970-1591.174774 PMID:27127351
• 4 Ghagane SC, Nerli RB, Hiremath MB, Wagh AT, Magdum PV. Incidence of prostate cancer at a single tertiary care center in North Karnataka. Indian J Cancer. 2016; 53:429–31. https://doi.org/10.4103/0019-509X.200671 PMID:28244476
• 5 Ganesh B, Saoba SL, Sarade MN, Pinjari SV. Risk factors for prostate cancer: An hospital-based case-control study from Mumbai, India. Indian J Urol. 2011; 27:345–50. https://doi.org/10.4103/0970-1591.85438 PMID:22022057
• 6 Macke AJ, Petrosyan A. Alcohol and Prostate Cancer: Time to Draw Conclusions. Biomolecules. 2022; 12:375. https://doi.org/10.3390/biom12030375 PMID:35327568
• 7 Ha Chung B, Horie S, Chiong E. The incidence, mortality, and risk factors of prostate cancer in Asian men. Prostate Int. 2019; 7:1–8. https://doi.org/10.1016/j.prnil.2018.11.001 PMID:30937291
• 8 Krstev S, Knutsson A. Occupational Risk Factors for Prostate Cancer: A Meta-analysis. J Cancer Prev. 2019; 24:91–111. https://doi.org/10.15430/JCP.2019.24.2.91 PMID:31360689
• 9 Rumgay H, Murphy N, Ferrari P, Soerjomataram I. Alcohol and Cancer: Epidemiology and Biological Mechanisms. Nutrients. 2021; 13:3173. https://doi.org/10.3390/nu13093173 PMID:34579050
• 10 Fan H, Xia S, Xiang J, Li Y, Ross MO, Lim SA, Yang F, Tu J, Xie L, Dougherty U, Zhang FQ, Zheng Z, Zhang R, et al. Trans-vaccenic acid reprograms CD8+ T cells and antitumour immunity. Nature. 2023; 623:1034–43. https://doi.org/10.1038/s41586-023-06749-3 PMID:37993715
• 11 Joosen AM, Kuhnle GG, Aspinall SM, Barrow TM, Lecommandeur E, Azqueta A, Collins AR, Bingham SA. Effect of processed and red meat on endogenous nitrosation and DNA damage. Carcinogenesis. 2009; 30:1402–7. https://doi.org/10.1093/carcin/bgp130 PMID:19498009
• 12 John EM, Stern MC, Sinha R, Koo J. Meat consumption, cooking practices, meat mutagens, and risk of prostate cancer. Nutr Cancer. 2011; 63:525–37. https://doi.org/10.1080/01635581.2011.539311 PMID:21526454
• 13 Tuli HS, Garg VK, Bhushan S, Uttam V, Sharma U, Jain A, Sak K, Yadav V, Lorenzo JM, Dhama K, Behl T, Sethi G. Natural flavonoids exhibit potent anticancer activity by targeting microRNAs in cancer: A signature step hinting towards clinical perfection. Transl Oncol. 2023; 27:101596. https://doi.org/10.1016/j.tranon.2022.101596 PMID:36473401
• 14 Wang M, Yu F, Zhang Y, Chang W, Zhou M. The Effects and Mechanisms of Flavonoids on Cancer Prevention and Therapy: Focus on Gut Microbiota. Int J Biol Sci. 2022; 18:1451–75. https://doi.org/10.7150/ijbs.68170 PMID:35280689
• 15 Li X, Yu C, Guo Y, Bian Z, Shen Z, Yang L, Chen Y, Wei Y, Zhang H, Qiu Z, Chen J, Chen F, Chen Z, et al, and China Kadoorie Biobank Collaborative Group. Association between tea consumption and risk of cancer: a prospective cohort study of 0.5 million Chinese adults. Eur J Epidemiol. 2019; 34:753–63. https://doi.org/10.1007/s10654-01900530-5 PMID:31152367
• 16 Cavin C, Marin-Kuan M, Langouët S, Bezençon C, Guignard G, Verguet C, Piguet D, Holzhäuser D, Cornaz R, Schilter B. Induction of Nrf2-mediated cellular defenses and alteration of phase I activities as mechanisms of chemoprotective effects of coffee in the liver. Food Chem Toxicol. 2008; 46:1239–48. https://doi.org/10.1016/j.fct.2007.09.099 PMID:17976884
• 17 Islam MT, Tabrez S, Jabir NR, Ali M, Kamal MA, da Silva Araujo L, De Oliveira Santos JV, Da Mata AMO, De Aguiar RPS, de Carvalho Melo Cavalcante AA. An Insight into the Therapeutic Potential of Major Coffee Components. Curr Drug Metab. 2018; 19:544–56. https://doi.org/10.2174/1389200219666180302154551 PMID:29512445
• 18 Montenegro J, Freitas-Silva O, Teodoro AJ. Molecular Mechanisms of Coffee on Prostate Cancer Prevention. Biomed Res Int. 2022; 2022:3254420. https://doi.org/10.1155/2022/3254420 PMID:35496060
• 19 Zu K, Giovannucci E. Smoking and aggressive prostate cancer: a review of the epidemiologic evidence. Cancer Causes Control. 2009; 20:1799–810. https://doi.org/10.1007/s10552-009-9387-y PMID:19562492
• 20 Moreira DM, Nickel JC, Gerber L, Muller RL, Andriole GL, Castro-Santamaria R, Freedland SJ. Smoking Is Associated with Acute and Chronic Prostatic Inflammation: Results from the REDUCE Study. Cancer Prev Res (Phila). 2015; 8:312–17. https://doi.org/10.1158/1940-6207.CAPR-140260 PMID:25644151
• 21 Ishida M, Sakai C, Kobayashi Y, Ishida T. Cigarette Smoking and Atherosclerotic Cardiovascular Disease. J Atheroscler Thromb. 2024; 31:189–200. https://doi.org/10.5551/jat.RV22015 PMID:38220184
• 22 Xu H, Liu C, Gu M, Chen Y, Cai Z, Chen Q, Wang Z. Prostatic vascular damage induced by cigarette smoking as a risk factor for recovery after holmium laser enucleation of the prostate (HoLEP). Oncotarget. 2017; 8:14039–49. https://doi.org/10.18632/oncotarget.12538 PMID:27732940
• 23 Rodu B, Godshall WT. Tobacco harm reduction: an alternative cessation strategy for inveterate smokers. Harm Reduct J. 2006; 3:37. https://doi.org/10.1186/1477-7517-337 PMID:17184539
• 24 Henley SJ, King JB, German RR, Richardson LC, Plescia M, and Centers for Disease Control and Prevention (CDC). Surveillance of screening-detected cancers (colon and rectum, breast, and cervix) - United States, 2004-2006. MMWR Surveill Summ. 2010; 59:1–25. PMID:21102407
• 25 Dwivedi S, Goel A, Mandhani A, Khattri S, Pant KK. Tobacco exposure may enhance inflammation in prostate carcinoma patients: an explorative study in north Indian population. Toxicol Int. 2012; 19:310–18. https://doi.org/10.4103/0971-6580.103681 PMID:23293472
• 26 Koutros S, Beane Freeman LE, Lubin JH, Heltshe SL, Andreotti G, Barry KH, DellaValle CT, Hoppin JA, Sandler DP, Lynch CF, Blair A, Alavanja MC. Risk of total and aggressive prostate cancer and pesticide use in the Agricultural Health Study. Am J Epidemiol. 2013; 177:59–74. https://doi.org/10.1093/aje/kws225 PMID:23171882
• 27 Corti M, Lorenzetti S, Ubaldi A, Zilli R, Marcoccia D. Endocrine Disruptors and Prostate Cancer. Int J Mol Sci. 2022; 23:1216. https://doi.org/10.3390/ijms23031216 PMID:35163140
• 28 Cockburn M, Mills P, Zhang X, Zadnick J, Goldberg D, Ritz B. Prostate cancer and ambient pesticide exposure in agriculturally intensive areas in California. Am J Epidemiol. 2011; 173:1280–88. https://doi.org/10.1093/aje/kwr003 PMID:21447478
• 29 Parent ME, Désy M, Siemiatycki J. Does exposure to agricultural chemicals increase the risk of prostate cancer among farmers? Mcgill J Med. 2009; 12:70–77. PMID:19753293
• 30 Singhavi HR, Singh A, Bhattacharjee A, Talole S, Dikshit R, Chaturvedi P. Alcohol and cancer risk: A systematic review and meta-analysis of prospective Indian studies. Indian J Public Health. 2020; 64:186–90. https://doi.org/10.4103/ijph.IJPH_529_19 PMID:32584303
• 31 Tyagi B, Manoharan N, Raina V. A case control study on prostate cancer in Delhi. Asian Pac J Cancer Prev. 2010; 11:397–401. PMID:20843123
• 32 Bagnardi V, Rota M, Botteri E, Tramacere I, Islami F, Fedirko V, Scotti L, Jenab M, Turati F, Pasquali E, Pelucchi C, Galeone C, Bellocco R, et al. Alcohol consumption and site-specific cancer risk: a comprehensive dose-response meta-analysis. Br J Cancer. 2015; 112:580–93. https://doi.org/10.1038/bjc.2014.579 PMID:25422909
• 33 Zhao J, Stockwell T, Roemer A, Chikritzhs T. Is alcohol consumption a risk factor for prostate cancer? A systematic review and meta-analysis. BMC Cancer. 2016; 16:845. https://doi.org/10.1186/s12885-016-2891-z PMID:27842506
• 34 Vartolomei MD, Kimura S, Ferro M, Foerster B, Abufaraj M, Briganti A, Karakiewicz PI, Shariat SF. The impact of moderate wine consumption on the risk of developing prostate cancer. Clin Epidemiol. 2018; 10:431–44. https://doi.org/10.2147/CLEP.S163668 PMID:29713200
• 35 D’Ecclesiis O, Pastore E, Gandini S, Caini S, Marvaso G, Jereczek-Fossa BA, Corrao G, Raimondi S, Bellerba F, Ciceri S, Latella M, Cavalcabò NB, Bendinelli B, et al. Association between Alcohol Intake and Prostate Cancer Mortality and Survival. Nutrients. 2023; 15:925. https://doi.org/10.3390/nu15040925 PMID:36839283
• 36 Wilson KM, Mucci LA, Drake BF, Preston MA, Stampfer MJ, Giovannucci E, Kibel AS. Meat, Fish, Poultry, and Egg Intake at Diagnosis and Risk of Prostate Cancer Progression. Cancer Prev Res (Phila). 2016; 9:933–41. https://doi.org/10.1158/1940-6207.CAPR-16-0070 PMID:27651069
• 37 He Q, Wan ZC, Xu XB, Wu J, Xiong GL. Poultry consumption and prostate cancer risk: a meta-analysis. PeerJ. 2016; 4:e1646. https://doi.org/10.7717/peerj.1646 PMID:26855875
• 38 Bylsma LC, Alexander DD. A review and meta-analysis of prospective studies of red and processed meat, meat cooking methods, heme iron, heterocyclic amines and prostate cancer. Nutr J. 2015; 14:125. https://doi.org/10.1186/s12937-015-0111-3 PMID:26689289
• 39 Gilsing AM, Weijenberg MP, Goldbohm RA, Dagnelie PC, van den Brandt PA, Schouten LJ. Vegetarianism, low meat consumption and the risk of lung, postmenopausal breast and prostate cancer in a population-based cohort study. Eur J Clin Nutr. 2016; 70:723–29. https://doi.org/10.1038/ejcn.2016.25 PMID:26931668
• 40 Nouri-Majd S, Salari-Moghaddam A, Aminianfar A, Larijani B, Esmaillzadeh A. Association Between Red and Processed Meat Consumption and Risk of Prostate Cancer: A Systematic Review and Meta-Analysis. Front Nutr. 2022; 9:801722. https://doi.org/10.3389/fnut.2022.801722 PMID:35198587
• 41 Zuniga KB, Chan JM, Ryan CJ, Kenfield SA. Diet and lifestyle considerations for patients with prostate cancer. Urol Oncol. 2020; 38:105–17. https://doi.org/10.1016/j.urolonc.2019.06.018 PMID:31327752
• 42 Bahrami A, Movahed M, Teymoori F, Mazandaranian MR, Rashidkhani B, Hekmatdoost A, Hejazi E. Dietary Nutrient Patterns and Prostate Cancer Risk: A Case-Control Study from Iran. Asian Pac J Cancer Prev. 2019; 20:1415–20. https://doi.org/10.31557/APJCP.2019.20.5.1415 PMID:31127901
• 43 Geybels MS, Neuhouser ML, Stanford JL. Associations of tea and coffee consumption with prostate cancer risk. Cancer Causes Control. 2013; 24:941–48. https://doi.org/10.1007/s10552-013-0170-8 PMID:23412806
• 44 Thomas R, Greef B, McConnachie A, Stanley B, Williams M. Dietary consumption of tea and the risk of prostate cancer in the Prostate, Lung, Colorectal and Ovarian Cancer Screening Trial. Br J Nutr. 2022; 128:653–58. https://doi.org/10.1017/S0007114521003664 PMID:34511161
• 45 Lin YW, Hu ZH, Wang X, Mao QQ, Qin J, Zheng XY, Xie LP. Tea consumption and prostate cancer: an updated meta-analysis. World J Surg Oncol. 2014; 12:38. https://doi.org/10.1186/1477-7819-12-38 PMID:24528523
• 46 Montague JA, Butler LM, Wu AH, Genkinger JM, Koh WP, Wong AS, Wang R, Yuan JM, Yu MC. Green and black tea intake in relation to prostate cancer risk among Singapore Chinese. Cancer Causes Control. 2012; 23:1635–41. https://doi.org/10.1007/s10552-012-0041-8 PMID:22864870
• 47 Lee PMY, Ng CF, Liu ZM, Ho WM, Lee MK, Wang F, Kan HD, He YH, Ng SSM, Wong SYS, Tse LA. Reduced prostate cancer risk with green tea and epigallocatechin 3-gallate intake among Hong Kong Chinese men. Prostate Cancer Prostatic Dis. 2017; 20:318–22. https://doi.org/10.1038/pcan.2017.18 PMID:28417981
• 48 Guo Y, Zhi F, Chen P, Zhao K, Xiang H, Mao Q, Wang X, Zhang X. Green tea and the risk of prostate cancer: A systematic review and meta-analysis. Medicine (Baltimore). 2017; 96:e6426. https://doi.org/10.1097/MD.0000000000006426 PMID:28353571
• 49 Mak JC. Potential role of green tea catechins in various disease therapies: progress and promise. Clin Exp Pharmacol Physiol. 2012; 39:265–73. https://doi.org/10.1111/j.1440-1681.2012.05673.x PMID:22229384
• 50 Chen X, Zhao Y, Tao Z, Wang K. Coffee consumption and risk of prostate cancer: a systematic review and meta-analysis. BMJ Open. 2021; 11:e038902. https://doi.org/10.1136/bmjopen-2020-038902 PMID:33431520
• 51 Liu H, Hu GH, Wang XC, Huang TB, Xu L, Lai P, Guo ZF, Xu YF. Coffee consumption and prostate cancer risk: a meta-analysis of cohort studies. Nutr Cancer. 2015; 67:392–400. https://doi.org/10.1080/01635581.2015.1004727 PMID:25706900
• 52 Wilson KM, Kasperzyk JL, Rider JR, Kenfield S, van Dam RM, Stampfer MJ, Giovannucci E, Mucci LA. Coffee consumption and prostate cancer risk and progression in the Health Professionals Follow-up Study. J Natl Cancer Inst. 2011; 103:876–84. https://doi.org/10.1093/jnci/djr151 PMID:21586702
• 53 Shafique K, McLoone P, Qureshi K, Leung H, Hart C, Morrison DS. Coffee consumption and prostate cancer risk: further evidence for inverse relationship. Nutr J. 2012; 11:42. https://doi.org/10.1186/1475-2891-11-42 PMID:22695052
• 54 Zhong S, Chen W, Yu X, Chen Z, Hu Q, Zhao J. Coffee consumption and risk of prostate cancer: an up-to-date meta-analysis. Eur J Clin Nutr. 2014; 68:330–37. https://doi.org/10.1038/ejcn.2013.256 PMID:24300907
• 55 Lotufo PA, Lee IM, Ajani UA, Hennekens CH, Manson JE. Cigarette smoking and risk of prostate cancer in the physicians’ health study (United States). Int J Cancer. 2000; 87:141–44. https://doi.org/10.1002/10970215(20000701)87:1<141::aid-ijc21>3.0.co;2-a PMID:10861465
• 56 Yang X, Chen H, Zhang S, Chen X, Sheng Y, Pang J. Association of cigarette smoking habits with the risk of prostate cancer: a systematic review and meta-analysis. BMC Public Health. 2023; 23:1150. https://doi.org/10.1186/s12889-023-16085-w PMID:37316851
• 57 Plaskon LA, Penson DF, Vaughan TL, Stanford JL. Cigarette smoking and risk of prostate cancer in middleaged men. Cancer Epidemiol Biomarkers Prev. 2003; 12:604–9. PMID:12869398
• 58 Jochems SHJ, Fritz J, Häggström C, Järvholm B, Stattin P, Stocks T. Smoking and Risk of Prostate Cancer and Prostate Cancer Death: A Pooled Study. Eur Urol. 2023; 83:422–31. https://doi.org/10.1016/j.eururo.2022.03.033 PMID:35523620
• 59 De Nunzio C, Andriole GL, Thompson IM Jr, Freedland SJ. Smoking and Prostate Cancer: A Systematic Review. Eur Urol Focus. 2015; 1:28–38. https://doi.org/10.1016/j.euf.2014.10.002 PMID:28723351
• 60 Pandey A, Singh A, Singh S, Kumar A, Das A, Shahi H, Singh A. Oral smokeless tobacco consumption pattern among rural Indian cancer patients: A prospective survey. South Asian J Cancer. 2020; 9:17–19. https://doi.org/10.4103/sajc.sajc_40_19 PMID:31956612
• 61 Lyon F. Description of Smokeless Tobacco Practices. America. 2007; 89:41–165. https://www.ncbi.nlm.nih.gov/books/NBK326503/
• 62 Gupta S, Gupta R, Sinha DN, Mehrotra R. Relationship between type of smokeless tobacco & risk of cancer: A systematic review. Indian J Med Res. 2018; 148:56–76. https://doi.org/10.4103/ijmr.IJMR_2023_17 PMID:30264755
• 63 Ramadas K, Sauvaget C, Thomas G, Fayette JM, Thara S, Sankaranarayanan R. Effect of tobacco chewing, tobacco smoking and alcohol on all-cause and cancer mortality: a cohort study from Trivandrum, India. Cancer Epidemiol. 2010; 34:405–12. https://doi.org/10.1016/j.canep.2010.04.006 PMID:20444665
• 64 Gupta PC, Arora M, Sinha DN, Asma S. Smokeless Tobacco and Public Health in India. Ministry of Health and Family Welfare, Government of India. 2016. https://ntcp.mohfw.gov.in/assets/document/surveys-reports-publications/SmokelessTobacco-and-Public-Health-in-India.pdf
• 65 Chandrupatla SG, Tavares M, Natto ZS. Tobacco Use and Effects of Professional Advice on Smoking Cessation among Youth in India. Asian Pac J Cancer Prev. 2017; 18:1861–67. https://doi.org/10.22034/APJCP.2017.18.7.1861 PMID:28749122
• 66 Pardo LA, Beane Freeman LE, Lerro CC, Andreotti G, Hofmann JN, Parks CG, Sandler DP, Lubin JH, Blair A, Koutros S. Pesticide exposure and risk of aggressive prostate cancer among private pesticide applicators. Environ Health. 2020; 19:30. https://doi.org/10.1186/s12940-02000583-0 PMID:32138787
• 67 Band PR, Abanto Z, Bert J, Lang B, Fang R, Gallagher RP, Le ND. Prostate cancer risk and exposure to pesticides in British Columbia farmers. Prostate. 2011; 71:168–83. https://doi.org/10.1002/pros.21232 PMID:20799287
• 68 Dosemeci M, Hoover RN, Blair A, Figgs LW, Devesa S, Grauman D, Fraumeni JF Jr. Farming and prostate cancer among African-Americans in the southeastern United States. J Natl Cancer Inst. 1994; 86:1718–19. https://doi.org/10.1093/jnci/86.22.1718 PMID:7966401
• 69 Acquavella J, Olsen G, Cole P, Ireland B, Kaneene J, Schuman S, Holden L. Cancer among farmers: a metaanalysis. Ann Epidemiol. 1998; 8:64–74. https://doi.org/10.1016/s1047-2797(97)00120-8 PMID:9465996
• 70 Van Maele-Fabry G, Willems JL. Occupation related pesticide exposure and cancer of the prostate: a metaanalysis. Occup Environ Med. 2003; 60:634–42. https://doi.org/10.1136/oem.60.9.634 PMID:12937183
• 71 Meyer TE, Coker AL, Sanderson M, Symanski E. A case-control study of farming and prostate cancer in AfricanAmerican and Caucasian men. Occup Environ Med. 2007; 64:155–60. https://doi.org/10.1136/oem.2006.027383 PMID:16912087
• 72 Krstev S, Baris D, Stewart P, Dosemeci M, Swanson GM, Greenberg RS, Schoenberg JB, Schwartz AG, Liff JM, Hayes RB. Occupational risk factors and prostate cancer in U.S. blacks and whites. Am J Ind Med. 1998; 34:421–30. https://doi.org/10.1002/(sici)1097-0274(199811)34:5<421::aidajim2>3.0.co;2-t PMID:9787845

Last Modified: 2026-04-28T17:18:25.717Z