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Review
Tea, Coffee and Prostate Cancer
Andy H. Lee, Michelle L. Fraser and Colin W. Binns
School of Public Health, Curtin University of Technology, Perth, WA, Australia
Worldwide, prostate cancer has the second highest incidence of all cancers in males with incidence and mortality being much higher in affluent developed countries. Risk and progression of the disease may be linked to both genetic and environmental factors, especially dietary factors. Tea and coffee are two of the most popular beverages in the world and have been investigated for possible effects on health outcomes, including cancer. However, very little dietary advice for their consumption exists. The evidence for a relationship between coffee or tea consumption and prostate cancer is reviewed in this paper. While current evidence indicates that coffee is a safe beverage, its consumption probably has no relationship with prostate cancer. Tea, especially green tea, has shown some potential in the prevention of prostate cancer. While evidence from epidemiologic studies is currently inconclusive, strong evidence has emerged from animal and in vitro studies. We also consider what level of evi- dence is required to make recommendations for preventive measures to the public. Although evidence on the relationship between coffee, tea and prostate cancer is not complete, we consider it strong enough to recommend tea as a healthier alternative to coffee.
Keywords: Coffee / Dietary guidelines / Epidemiologic studies / Prostate cancer / Tea /
Received: April 30, 2008; revised: June 2, 2008; accepted: June 5, 2008
1 Introduction
Worldwide, prostate cancer has the second highest inci- dence of all cancers in males [1] and in many developed countries, it is the most common neoplasm in men beyond middle age [2]. Prostate cancer incidence and mortality varies widely between geographic regions, with overall rates in high-income countries such as Australia and USA being nearly six times higher than in middle to low-income countries such as China, Japan, and African countries [1, 2]. However, the reported incidence in countries such as China is increasing rapidly [3]. This variation in incidence suggests that risk and progression of the disease may be linked to both genetic and environmental factors, especially dietary factors. Discovering possible chemopreventive diet- ary factors is important in the case of prostate cancer due to the aging populations of most Western nations. Prostate cancer is also an ideal candidate disease for chemopreven-
tion because relative survival after diagnosis is high [4] due to its long latency and typical detection in older men who usually have a slower rate of progression [2].
Tea and coffee are two popular beverages that have been investigated for possible effects on health outcomes, includ- ing cancer. Coffee was once suspected of increasing the risk of various cancers [5] whereas tea, especially green tea has shown promise in the prevention of cancers including gas- trointestinal tract [6 – 8], skin [9, 10], breast [11 – 13], pan- creas, esophagus, and lung [14]. Epidemiological studies on tea and prostate cancer have generated inconsistent results [15], however a recent Chinese case-control study reported a significant dose response relationship between green tea consumption and prostate cancer risk [16].
Despite coffee and tea being two of the most commonly consumed beverages all over the world [17], very little diet- ary advice for their consumption exists. Recently, several reviews have addressed the potential relationship between tea and prostate cancer prevention [18 – 20]. Although they have concluded that tea or tea compounds show promise in prostate cancer prevention, little effort has been made to translate these findings into public health guidelines. This paper therefore, considers whether evidence is currently strong enough to make any dietary recommendations on tea or coffee and prostate cancer prevention by presenting the epidemiologic evidence as well as mechanistic evidence from in vitro and animal model studies.
Correspondence: Professor Colin W. Binns, School of Public Health, Curtin University of Technology, GPO Box U 1987, Perth, WA 6845, Australia E-mail: [email protected] Fax: +61-8-92662958
Abbreviations: CI, confidence interval; EGCG, ( – )epigallocatechin- 3-gallate; GTC, green tea catechin; OR, odds ratio; RCT, randomized controlled trial; RR, relative risk
i 2009 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim www.mnf-journal.com
DOI 10.1002/mnfr.200800218 Mol. Nutr. Food Res. 2009, 53, 256 – 265
Mol. Nutr. Food Res. 2009, 53, 256 – 265
2 Materials and methods
Published articles were located by searching the PubMed, CINAHL, and ProQuest databases with the keywords “tea” and “prostate cancer” and “coffee” and “prostate cancer” without any restriction on publication date. The corre- sponding reference lists were also searched for relevant articles. The National Health and Medical Research Coun- cil's Levels of Evidence for Clinical Practice Guidelines were used to divide and evaluate existing evidence for both coffee and tea [21]. The level of evidence refers to the study design used to minimize bias with the highest level involv- ing a systematic review of randomized controlled trials (RCTs), followed by at least one properly designed RCT, then pseudo- RCTs, then observational studies. Also con- sidered is evidence quality – methods used to minimize bias in the study design and conduct, evidence relevance – extent to which findings can be applied in other settings, and strength of evidence – magnitude and reliability of the treatment effect [21]. In addition, animal model and in vitro studies have been included to establish biological plausibil- ity of the observed effects.
3 Results
3.1 Coffee and tea: Patterns of consumption
Tea and coffee are two of the world's most popular bever- ages and both are consumed in most countries [17]. World- wide, tea consumption is second only to water and approxi- mately three cups of tea are drunk for every cup of coffee [17]. However, coffee is the preferred drink throughout the majority of Europe and the Americas with 71.5% of coffee consumption taking place in developed countries [17]. Tea consumption dominates in the developing world with 76.6% of consumption taking place in these countries [17]. Tea is also the more popular beverage in liters in Australia [22] and Britain [17]. Of the total tea produced and con- sumed, 78% is black, 20% green, and less than 2% oolong [23]. Black tea is primarily consumed in Western countries while green tea is mainly consumed in China, Japan, India, and a few countries in North Africa and the Middle East [23].
3.2 The composition of tea and coffee
Coffee is produced by infusing ground, roasted coffee beans, the most popular forms being Coffea arabica and C. canephoria var. robusta [17]. The three most common kinds of tea are green, black, and oolong tea and these are all derived from the Camellia sinensis plant [24]. Green tea leaves are steamed when harvested to prevent fermentation whereas black tea is fermented as leaves wither then are rolled and crushed. Oolong tea is partially fermented and considered to be about half as fermented as black tea [24].
Coffee and tea are both complex substances consisting of many compounds. Coffee is reported to contain more than a thousand different chemicals, several of which have been shown to have physiological effects [5]. The stimulatory effects of caffeine [25] and antioxidant activity of chloro- genic acid and caffeic acid have been extensively researched [26] and other micronutrients including magne- sium, potassium, niacin, and vitamin E have also been sus- pected of health effects [5].
Green, oolong, and black teas all contain potentially can- cer preventive compounds, however the different manufac- turing process changes the profile of these compounds con- siderably [24]. Polyphenols are the most researched compo- nent of tea. Most of the polyphenolic content of green tea is flavanols, know as catechins, including (–)-epicatechin, (–)-epicatechin-3-gallate, (–)epigallocatechin, and (–)epi- gallocatechin-3-gallate (EGCG) [24]. In black and oolong tea, the fermentation process results in oxidation of simple polyphenols to complex theaflavins and thearubigins and reduces the catechin content of black tea to approximately a third of that of green tea [24].
3.3 Coffee and prostate cancer: Epidemiologic evidence
Coffee has been studied extensively for relationships with various cancers. Early case-control studies indicated a pos- sible positive relationship between coffee consumption and several cancers [27, 28]. It is possible however, that the association between coffee drinking and other unhealthy behaviors such as smoking and lack of exercise generated these observations as subsequent studies have produced lit- tle evidence of any significant relationship with cancer [5].
The possible relationship between coffee and prostate cancer has been investigated in epidemiologic studies since the 1980s. We identified seven case-control [29 – 35] and four cohort studies [36 – 39] reporting on coffee consump- tion and prostate cancer risk and two cohort studies examin- ing prostate cancer mortality [40, 41]; see Table 1. Results of these studies were very inconsistent. Overall, no relation- ship has emerged with almost all studies reporting no asso- ciation or nonsignificant positive and nonsignificant inverse associations with prostate cancer. No dose-response relationship emerged from any of these studies and only one reported statistically significant results [29]. However, this hospital-based case-control study conducted in Taiwan, only quantified coffee consumption as “yes” or “no” and the number of coffee consumers in the sample was very low consisting of 31 cases (13.1%) and 36 controls (7.5%) [29]. It is also possible that consumption of coffee in this Taiwa- nese study was associated with other aspects of a Western diet that may increase cancer risk. Although many of the other studies quantified coffee consumption in more detail and were all conducted in North American and European populations where coffee drinking is more common, coffee
257
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A. H. Lee et al. Mol. Nutr. Food Res. 2009, 53, 256 – 265
was rarely the main focus of the dietary questionnaire. Hence, exposure misclassification including cup size and caffeine variation of particular coffees [42] as well as con- founding may have affected the results of these studies.
3.4 Coffee and prostate cancer: In vitro and animal evidence
A vast amount of research in animals and in vitro cell cul- tures has also generated inconsistent findings about the role of coffee and its components in cancer. Coffee contains large number of compounds, some of which have been identified as having potentially chemopreventive effects including caffeine [43], chlorogenic and caffeic acids [44] and the diterpenes cafestol and kahweol [45], and others, having potentially carcinogenic effects also including caf- feine and methylglyoxal [46].
Some early evidence from molecular, cellular, and animal studies indicated that coffee could inhibit relevant DNA
repair mechanisms, modify the apoptotic response and per- turb cell cycle checkpoint integrity [47, 48]. One study reported an association between coffee drinking and muta- tions in the K-ras gene in exocrine pancreatic cancer [49]. However, the majority of research has reported a wide range of chemopreventive effects [45, 46]. Recent in vitro and in vivo studies in rats have also shown that coffee can suppress proliferation and invasion, possibly by inducing cell cycle arrest, apoptosis and the invasion by scavenging ROS, and can ameliorate abnormal lipoprotein profiles [50].
It is possible that coffee may possess both mutagenic and antimutagenic potential. In the past there has been concern that coffee consumption may increase the risk of bladder and pancreatic cancer, however, two recent reviews have concluded that it is unlikely to have any substantial effect on risk [1, 51]. For all other cancers, the World Cancer Research Fund reported that evidence is too limited to draw a conclusion [1]. In light of all the evidence, coffee prob- ably has no relationship with the risk of prostate cancer.
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Table 1. Summary of epidemiologic studies of coffee and prostate cancer
Country Study design Sample size Coffee consumption level Results: Adjusted OR, RR (95% CI) or p for trend
Reference
Taiwan Case-control (hospital- based)
237 cases, 481 controls Coffee drinking versus non- drinking
OR: 1.88 (1.07 – 3.30) [29]
Canada Case-control (popula- tion-based)
399 cases, 476 popula- tion controls, 621 cancer controls
A119 drink years versus a57 drink yearsa)
OR: 1.1 (0.6 – 2.0) for population controls
[30]
Greece Case-control (hospital- based)
320 cases, 246 controls F3 cups/day versus none p for trend: 0.27 [31]
Canada Case-control (popula- tion-based)
1623 cases, 1623 controls
a1 cup/day versus none 1 – 3 cups/day versus none F4 cups/day versus none
OR: 0.8 (0.6 – 1.1) OR: 1.0 (0.7 – 1.3) OR: 1.1 (0.8 – 1.5)
[32]
Canada Case-control (popula- tion-based)
617 cases 637 controls 0 – 500 g/day versus none >500 g/day versus none
OR: 0.84 (0.58 – 1.22) OR: 0.97 (0.65 – 1.44)
[33]
Sweden Case-control (popula- tion-based)
406 cases, 1218 controls 1 – 2 cups/day versus none 3 – 5 cups/day versus none 6 – 9 cups/day versus none
OR: 1.77 (0.65 – 5.09) OR: 1.99 (0.78 – 5.46) OR: 1.91 (0.73 – 5.30)
[34]
USA (Utah) Case-control (popula- tion-based)
326 cases, 685 controls 1 – 20 cups/week versus none A20 cups/week versus none
OR: 0.99 (0.68 – 1.47) OR: 1.09 (0.75 – 1.60)
[35]
Canada Cohort (retrospective) 3400 (145 developed prostate cancer)
A250 mL/day versus none RR: 1.4 (0.84 – 2.32) [36]
USA (Hawaii) Cohort 20 316 (198 developed prostate cancer)
A2.5 cups/day versus none RR: 1.1 (0.7 – 1.7) [37]
USA (Hawaii) Cohort 7999 (174 developed prostate cancer)
2 – 4 cups/week versus f 1 cup/week F5 cup/week versus f1 cup/week
RR: 0.96 (0.39 – 2.37) RR: 0.92 (0.59 – 1.44)
[38]
USA (Hawaii) Cohort 7355 men, 108 prostate cancer
Not stated Not stated, no signifi- cant relationship ob- served
[39]
USA Cohort (examined mortality)
17 633 men, 149 died of prostate cancer
3 – 4 cups/day versus <3 cups/day F5 cups/day versus <3 cups/day
RR: 0.8 (0.6 – 1.2)
RR: 1.0 (0.6 – 1.6)
[40]
USA (California)
Cohort (examined mortality)
21 295 seventh day adventists, 113000 non adventists
Not stated Not stated, nonstatisti- cally significant inverse association
[41]
a) Drink years: average number of drinks daily multiplied by duration of drinking in years.
Mol. Nutr. Food Res. 2009, 53, 256 – 265 259
i 2009 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim www.mnf-journal.com
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A. H. Lee et al. Mol. Nutr. Food Res. 2009, 53, 256 – 265
3.5 Tea and prostate cancer: Epidemiologic evidence
Table 2 summarizes epidemiologic studies of tea and pros- tate cancer from the literature. A hospital-based case-control study in China, where green tea is predominantly consumed provides promising evidence for a role of tea in prostate can- cer prevention [16]. A total of 130 cases and 274 hospital inpatients without any malignant disease were interviewed in detail about the type, duration, quantity, and frequency of tea consumption. Compared to nontea drinkers, the odds ratio (OR) was 0.28 (95% confidence interval (CI): 0.17 – 0.47) for those drinking green tea, 0.12 (95% CI: 0.06 – 0.26) for drinking tea longer than 40 years, 0.09 (95% CI: 0.04 – 0.21) for consuming more than 1.5 kg of tea leaves per year, and 0.27 (95% CI: 0.15 – 0.48) for drinking more than three cups (1 L) daily. According to the US Food and Drug Admin- istration, this study received high methodological quality ratings [52]. Another hospital-based case control study of 140 cases and 140 controls in Japan reported an OR for drinking two to ten cups of green tea daily ranging from 0.67 to 0.99 [53], but did not attain statistical significance, prob- ably due to the small sample size [52].
A slight reduction in prostate cancer risk was also reported by a larger Canadian case-control study involving 617 cases and 637 population controls [33]. An OR of 0.70 (95% CI: 0.50 – 0.99) was reported with consumption of more than 500 g (approximately two cups) of tea per day [33]. Another case-control study conducted in Montreal, Canada [30] reported an increased risk and two conducted in Canada [32] and Utah, USA [35] reported no association between tea consumption and prostate cancer, although alternative explanations for the observed effects could not be ruled out [30].
Cohort studies have reported inconsistent results, how- ever a recent prospective cohort study in Japan reported a significant dose-dependant relationship between green tea consumption and reduced risk of advanced prostate cancer but no association with localized prostate cancer [54]. These findings suggest the effects of green tea may vary according to prostate cancer stage and are supported by ear- lier results of small clinical trials and animal model studies [55 – 57]. In the cohort study, the multivariate relative risk (RR) for advanced prostate cancer for consumption of five or more cups/day versus less than one cup was 0.52 (95% CI: 0.28 – 0.96) [54]. Another Japanese cohort study of 19 561 men (110 cases) reported a slight but nonsignificant decrease in risk [58]. The hazard ratio for consumption of five cups of green tea/day versus a 1/day was 0.85 (95% CI: 0.50 – 1.43). Another cohort of 7999 men of Japanese ancestry living in Hawaii showed a borderline significant increase in risk for green tea consumption, OR = 1.47 (95% CI: 0.99 – 2.19), but no association for black tea [38]. How- ever, an earlier cohort study involving 7833 Hawaii men of Japanese ancestry observed a weak albeit significant
inverse association between black tea intake and prostate cancer incidence, with RR being 0.6 for consuming more than one cup daily versus almost never [59]. Three subse- quent cohort studies conducted in the UK [60], Italy [61], and Canada [36] where black tea is predominantly con- sumed [23], found little association between tea consump- tion and prostate cancer incidence.
The epidemiologic evidence to date is limited in several aspects. Of the three studies reporting positive results [16, 53, 54] two were relatively small case-control study designs that are open to bias due to their retrospective design [52]. In addition, the majority of studies lacked comprehensive assessment of tea intake. For example, only six specified the type of tea consumed as green [16, 38, 53, 54, 58] or black [38, 53, 59]. Although green tea has produced more promis- ing results, only a small number of studies (5) specifically examined its consumption. Also, many studies did not com- prehensively assess level of tea intake, for example, one clas- sified consumption only as “never” or “ever” [38]. In addi- tion, few studies considered duration of tea drinking or the preparation method in their assessment. Various methodo- logical issues including the failure to control for potential confounding factors also could have affected the findings.
The possibly more promising results for green than black tea could be the result of several factors. The higher cate- chin content and antioxidant activity of green tea is one pos- sibility. Also, tea intake was considerably higher in the Chi- nese study [16] and prospective study in Japan [54] than any others, suggesting low consumption might explain the lack of significance elsewhere. In addition, confounding factors including Asian-style diets such as the consumption of soy products and certain vegetables, low fat and alcohol intake, as well as the small numbers of studies published may contribute.
3.6 Tea and prostate cancer: Clinical trials
A recent double blind placebo controlled study examined the effect of green tea catechins (GTCs) on high-risk men with high-grade prostate intraepithelial neoplasia [55]. Of the 30 men treated daily with GTC capsules, only one tumor was diagnosed after 1 year as opposed to nine tumors diagnosed in the 30 placebos. Despite the small sample, this study pro- vides the first evidence that GTC may possess potent in vivo chemopreventive activity in men prone to prostate cancer. Another small clinical trial reported minimal clinical activ- ity of green tea extract capsules in 15 men already diagnosed with hormone refractory prostate cancer [56].
3.7 Animal model studies on tea and prostate cancer
Consistent evidence has emerged from animal models for a protective effect of tea and its components against prostate
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cancer. Studies in the transgenic adenocarcinoma of the mouse prostate model have reported reduction in the devel- opment of prostate cancer with feeding of GTCs [57]. Apoptosis and significant inhibition of tumor development and metastasis was also reported with oral infusion of green tea polyphenols at a human dose equivalent to six cups of green tea per day [62] and with oral feeding of 0.1% GTC [63]. Injecting EGCG has also been shown to inhibit pros- tate cancer growth in nude mice [63]. In addition, black tea extract has recently showed a significant protective effect against testosterone induced oxidative injury in Wistar rat prostate [64]. Significant inhibition in growth of implanted prostate tumors in athymic nude mice and reduction in pros- tate specific antigen was also recently reported with treat- ment of water extract of black tea, theaflavins as well as green tea polyphenols [65].
3.8 In vitro cell culture studies on tea and prostate cancer
In vitro cell culture studies have consistently revealed bio- logically plausible mechanisms by which tea polyphenols and EGCG may affect the development or progression of prostate and other cancers. These components can inhibit cell growth and induce apoptosis through various pathways and can affect multiple cellular events [66].
3.8.1 Antioxidant properties of green tea Androgens induce oxidative stress, making them key fac- tors in prostate cancer development [64]. Catechins, espe- cially EGCG, are antioxidants or highly effective scav- engers of oxidizing molecules including singlet oxygen and various free radicals that many contribute to DNA damage and tumor promotion [67].
3.8.2 Modulation of cyclin kinase inhibitor One pathway by which cell growth is inhibited and apopto- sis induced is through the modulation of cyclin kinase inhibitor. Cyclins are over expressed in prostate cancer and EGCG has been shown to upregulate cyclin-dependent kin- ase inhibitors such as p21WAFI/CIPI [68 – 71], p27KIPI, p16INK4A, and p15INK4B and down modulate cyclin D1, cyclin E, cdk2, cdk4, and cdk6 [72].
3.8.3 Effects on proteasome activity EGCG has also been reported to be a proteasome inhibitor, capable of inducing growth arrest in tumor cells by inhibit- ing the system that allows cell – cycle progression and pro- tects tumor cells against apoptosis [73].
3.8.4 Alteration of gene expression Analysis of gene expression found that 25 genes in LNCaP cells, belonging to different regulatory pathways responded to treatment by EGCG [74]. It induced 16 growth inhibitory genes and repressed nine genes most of which belong to the
G-protein signaling network. The most prominent suppres- sion was of the PKC-agene [74]. Green tea polyphenols can also cause significant inhibition of insulin-like growth fac- tor in mice [62], while EGCG may influence the tumor sup- pressor gene p53 [70, 71].
3.8.5 Influence on enzymes EGCG has been shown to inhibit transcription factors including p53 and NF-jB. This leads to the activation of p21WAFI and Bax, changing the ratio of Bax to Bcl-2 and activating capases, enzymes that favor apoptosis [71]. Other enzymes also targeted by green tea polyphenols or EGCG include 5a-reductases [75], fatty acid synthase [76], cyclo- oxygenase-2 [72], urokinase-like plasminogen activator [68], ornithine decarboxylase [77], nitric-oxide synthase [78], mitogen-activated protein kinase [79], and matrix metalloproteinase [80]. A recent study suggests that activa- tion of ERK1/2 (a member of the mitogen-activated protein kinase family) is partially responsible for the antiprolifera- tive effects of EGCG [81].
4 Discussion
Despite coffee and tea being two of the most commonly consumed beverages in the world [17], very little dietary advice on their consumption exists. In the case of coffee, this review of epidemiologic, animal and in vitro evidence indicates that coffee consumption probably has no relation- ship with the risk of prostate cancer. A recent review from the World Cancer Research Fund/American Institute for Cancer Research also stated the level of evidence for effects of coffee on prostate cancer as “limited- no conclusion” [1]. Research to date agrees that coffee consumption is safe for healthy adults [25] but probably has no preventive effects on chronic diseases including cancers [5] and cardiovascu- lar disease [82 – 84].Tea is also a safe beverage but tea and its components, especially green tea have shown promise in the prevention of prostate cancer in animal and in vitro stud- ies, in some epidemiological studies and a small clinical trial. Evidence also exists for a possible preventive role of tea for other cancers [85 – 87] and cardiovascular disease [88 – 90].Current evidence for a role of tea in prostate can- cer prevention however, is definitely not conclusive and fur- ther studies are warranted [1, 91]. The inverse relationships reported by the Japanese prospective study [54] and Chi- nese case-control study [16] are promising but have not been replicated. Case-control studies, in particular are sub- ject to bias due to their retrospective design [52]. Consistent results have also been reported in animal and in vitro studies but these effects are not always reproducible in humans. Also, different types and brands of tea vary greatly in terms of their polyphenol profiles and content [92] and animal and in vitro studies often use very high concentrations of tea compounds that may not reflect the actual levels found in
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the human body after ingestion [93]. The oral bioavailabil- ity of GTCs is low and the effective concentration levels determined in in vitro studies are many fold more than the resulting systemic levels in humans meaning in vitro effects should be interpreted with caution [19, 94].
The National Health and Medical Research Council's hierarchy of evidence describes a meta-analysis or pooled analysis of data from a number of RCTs as the gold standard for clinical practice guidelines [21]. However, the bulk of evidence on tea and prostate cancer comes from epidemio- logical as well as animal and in vitro studies, meaning the level of evidence cannot rise above level III. Kroke et al. [95] acknowledge that reaching this gold standard is usually unrealistic when making recommendations for preventive rather than therapeutic measures. Using RCTs to evaluate the effect of lifetime tea drinking on the prostate cancer risk would be difficult and expensive. It would be difficult to use controls due to the impracticality of blinding and ran- domizing them and the long latency of prostate cancer. Prostate cancer is usually diagnosed in men aged over 65 [1]. However, these factors also make this cancer an ideal candidate for chemoprevention. Considering this, future research should utilize a variety of observational study designs and strengthen current evidence through shorter- term RCTs that examine the effects of tea consumption on prostate cancer development in men with premalignant lesions.It is clear that current evidence is not nearly strong enough to make recommendations when standards for ther- apeutic substances are considered. However, if nutritionists are asked to recommend either tea or coffee as the healthier option, we believe evidence is sufficient to recommend tea over coffee. World trends indicate that consumption is mov- ing away from tea toward coffee. This is the case, for exam- ple, in Australia [22]; see Table 3. In addition, the aging population of many developed countries means the inci- dence of prostate cancer and other chronic diseases is likely to increase. Therefore, waiting decades for more complete evidence to emerge before making any dietary guidelines on tea and coffee could result in unnecessary morbidity and mortality. Tea is both a safe and popular beverage, its pro- posed health effects are biologically plausible and recom- mending its consumption is not inconsistent with any pre- vious public health advice. These factors make it suitable to create dietary guidelines recommending the consumption of tea as a healthier choice than coffee [96].
Evidence on the dosage of tea required for effect, the efficacy of absorption in the human body and the different
chemopreventive effects of green, black, and oolong teas is required before any specific and quantifiable dietary guide- lines regarding tea consumption and prevention of prostate and other cancers can be made.
The authors have declared no conflict of interest.
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