Impact of Meat Consumption, Preparation, and Mutagens on Aggressive Prostate Cancer

Department of Urology, University of California San Francisco, San Francisco, California, United States of America.
PLoS ONE (Impact Factor: 3.23). 11/2011; 6(11):e27711. DOI: 10.1371/journal.pone.0027711
Source: PubMed


The association between meat consumption and prostate cancer remains unclear, perhaps reflecting heterogeneity in the types of tumors studied and the method of meat preparation--which can impact the production of carcinogens.
We address both issues in this case-control study focused on aggressive prostate cancer (470 cases and 512 controls), where men reported not only their meat intake but also their meat preparation and doneness level on a semi-quantitative food-frequency questionnaire. Associations between overall and grilled meat consumption, doneness level, ensuing carcinogens and aggressive prostate cancer were assessed using multivariate logistic regression.
Higher consumption of any ground beef or processed meats were positively associated with aggressive prostate cancer, with ground beef showing the strongest association (OR = 2.30, 95% CI:1.39-3.81; P-trend = 0.002). This association primarily reflected intake of grilled or barbequed meat, with more well-done meat conferring a higher risk of aggressive prostate cancer. Comparing high and low consumptions of well/very well cooked ground beef to no consumption gave OR's of 2.04 (95% CI:1.41-2.96) and 1.51 (95% CI:1.06-2.14), respectively. In contrast, consumption of rare/medium cooked ground beef was not associated with aggressive prostate cancer. Looking at meat mutagens produced by cooking at high temperatures, we detected an increased risk with 2-amino-3,8-Dimethylimidazo-[4,5-f]Quinolaxine (MelQx) and 2-amino-3,4,8-trimethylimidazo(4,5-f)qunioxaline (DiMelQx), when comparing the highest to lowest quartiles of intake: OR = 1.69 (95% CI:1.08-2.64;P-trend = 0.02) and OR = 1.53 (95% CI:1.00-2.35; P-trend = 0.005), respectively.
Higher intake of well-done grilled or barbequed red meat and ensuing carcinogens could increase the risk of aggressive prostate cancer.

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Available from: Jill Hardin, Sep 11, 2014
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    • "However, the results of two meta-analyses of the relation between dairy product intake and PC provided conflicting conclusions: one showed a significantly positive association (Gao et al., 2005) and the other (supported by the National Dairy Council) showed an overall null association (Huncharek et al., 2008). High consumption of meat has been also associated with PC risk (John et al., 2011; Punnen et al., 2011). The amount and type of fats consumed are also clearly related to PC risk (Patel, 2014). "
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    ABSTRACT: The aim of the present study was to determine the association between the socio-demographic, lifestyle factors, and dietary habits with the risk of prostate cancer (PC) in a case-control study of Spanish men. None of the socio-demographic, lifestyle or dietetic variables was found predictors of PC risk. Body mass index was associated with an increased risk for aggressive PC and fruit consumption with lower Gleason scores, thus less aggressive cancers. Nonetheless, after applying Bonferroni correction, these variables were not still associated with PC aggressiveness. More adequately, powered epidemiological studies that measure the effect of lifestyle and dietary intake in PC risk and aggressiveness are warranted to further elucidate the role of these modifiable factors on PC etiology.
    International Journal of Food Sciences and Nutrition 09/2015; DOI:10.3109/09637486.2015.1077786 · 1.21 Impact Factor
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    • "A high intake dose–response relation was found for intake of very well-done meat and exposure to PhIP [12]. In another cohort study conducted in the United States, a positive association was also found between high intake of well or very well-done meat and more aggressive prostate cancer [13]. "
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    ABSTRACT: Prostate cancer is the second most common cause of cancer worldwide after lung cancer. There is increasing evidence that diet and lifestyle plays a crucial role in prostate cancer biology and tumourigenesis. Prostate cancer itself represents a good model of cancer in which to look for chemopreventive agents due to the high disease prevalence, slowly progressive nature, and long latency period. Dietary agents have gained considerable attention, often receiving much publicity in the media. To review the key evidence available for potential chemopreventive nutrients. The methodology for this review involved a PubMed search from 1990 to 2013 using the key-words “diet and prostate cancer”, “nutrition and prostate cancer”, “dietary factors and prostate cancer”, “prostate cancer epidemiology”, “prostate cancer prevention”, “prostate cancer progression”. Red meat, dietary fat and milk intake should be minimised as they appear to increase the risk of prostate cancer. Fruit and vegetables and polyphenols may be preventive in prostate cancer, but further studies are needed to draw more solid conclusions and to clarify their role in patients with an established diagnosis of prostate cancer. Selenium and vitamin supplements cannot be advocated for the prevention of prostate cancer and indeed higher doses may be associated with a worse prognosis. There is no specific evidence regarding benefits of probiotics or prebiotics in prostate cancer. From the wealth of evidence available, many recommendations can be made although more randomised control trials are required. These need to be carefully designed due to the many confounding factors and heterogeneity of the population.
    Nutrition & Metabolism 06/2014; 11(1):30. DOI:10.1186/1743-7075-11-30 · 3.26 Impact Factor
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    • "However, dietary and lifestyle factors may also influence prostate cancer susceptibility [3,6]. Intake of red meat [7-10], dairy products [11,12], eggs [9,13,14], green tea [15,16], calcium [17-20], lycopene [21-23], selenium [6,24], and fish oil [4,25] have all been examined in relation to prostate cancer risk with relatively inconsistent results. The inconsistency of these findings may partly be due to the use of food intake measures as surrogates for bioavailable micronutrient levels, resulting in some misclassification of nutrient/metabolite exposures [26,27]. "
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    ABSTRACT: Among men in the U.S., prostate cancer is the most common cancer and the second leading cause of cancer death. Despite its prevalence, there are few established risk factors for prostate cancer. Some studies have found that intake of certain foods/nutrients may be associated with prostate cancer risk, but few have accounted for how intake and metabolic factors may interact to influence bioavailable nutrient levels and subsequent disease risk. The composition of the gastrointestinal (GI) microbiome may influence metabolism of dietary compounds and nutrients (e.g., plant phenols, calcium, choline) that may be relevant to prostate cancer risk. We, therefore, propose the hypothesis that GI microbiota may have a markedly different composition among individuals with higher prostate cancer risk. These individuals could have microbial profiles that are conducive to intestinal inflammation and/or are less favorable for the metabolism and uptake of chemopreventive agents. Because very little preliminary data exist on this potential association, a case--control study may provide valuable information on this topic. Such a study could evaluate whether the GI microbial profile is markedly different between three groups of individuals: healthy men, those with latent prostate cancer, and those with invasive prostate cancer. Any findings could then be validated in a larger study, designed to collect a series of specimens over time. Given the plethora of information emerging from the Human Microbiome Project, this is an opportune time to explore associations between the microbiome and complex human diseases. Identification of profiles that alter the host's risk for disease may clarify inconsistencies in the literature on dietary factors and cancer risk, and could provide valuable targets for novel cancer prevention strategies.
    Infectious Agents and Cancer 11/2013; 8(1):42. DOI:10.1186/1750-9378-8-42 · 2.36 Impact Factor
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