Abstract
It has been a long-standing debate in the research and medical societies whether alcohol consumption is linked to the risk of prostate cancer (PCa). Many comprehensive studies from different geographical areas and nationalities have shown that moderate and heavy drinking is positively correlated with the development of PCa. Nevertheless, some observations could not confirm that such a correlation exists; some even suggest that wine consumption could prevent or slow prostate tumor growth. Here, we have rigorously analyzed the evidence both for and against the role of alcohol in PCa development. We found that many of the epidemiological studies did not consider other, potentially critical, factors, including diet (especially, low intake of fish, vegetables and linoleic acid, and excessive use of red meat), smoking, family history of PCa, low physical activity, history of high sexual activities especially with early age of first intercourse, and sexually transmitted infections. In addition, discrepancies between observations come from selectivity criteria for control groups, questionnaires about the type and dosage of alcohol, and misreported alcohol consumption. The lifetime history of alcohol consumption is critical given that a prostate tumor is typically slow-growing; however, many epidemiological observations that show no association monitored only current or relatively recent drinking status. Nevertheless, the overall conclusion is that high alcohol intake, especially binge drinking, is associated with increased risk for PCa, and this effect is not limited to any type of beverage. Alcohol consumption is also directly linked to PCa lethality as it may accelerate the growth of prostate tumors and significantly shorten the time for the progression to metastatic PCa. Thus, we recommend immediately quitting alcohol for patients diagnosed with PCa. We discuss the features of alcohol metabolism in the prostate tissue and the damaging effect of ethanol metabolites on intracellular organization and trafficking. In addition, we review the impact of alcohol consumption on prostate-specific antigen level and the risk for benign prostatic hyperplasia. Lastly, we highlight the known mechanisms of alcohol interference in prostate carcinogenesis and the possible side effects of alcohol during androgen deprivation therapy.
Highlights
Introduction published maps and institutional affilThe link between alcohol consumption and malignant diseases has long intrigued researchers
We recently reported that in androgen-responsive prostate cancers (PCa) cells exposed to EtOH, Golgi disorganization is triggered by ACH and results in enhanced anchorage-independent growth, adherence, migration, and secretion of prostate specific antigen (PSA) [205]
At this point, there is no clear understanding of how EtOH accelerates the development of castration-resistant prostate cancer (CRPC), where the tumor no longer completely responds to androgen deprivation therapy (ADT)
Summary
Genetic sensitivity to alcohol’s influence on cancer can be explained by functional variation in alcohol metabolism genes [9]. ALDH catalyzes the production of retinoic acid, which was shown to block prostate tumorigenesis [33,34] This still does not rule out ACH accumulation in cancer cells because the rise in ADH activity may be more prominent than that of ALDH. Excessive alcohol consumption may induce the second pathway of EtOH metabolism: its oxidation in microsomes by cytochrome P450 2E1 (CYP2E1) enzyme (Figure 1) This pathway results in ROS production, which, in turn, may promote oxidative stress and subsequent DNA damage. Enhanced activity of ALDH enzymes results in excessive acetate production, which can be converted to acetyl CoA The latter reaction provides an uncontrolled amount of adenosine monophosphate (AMP), the degradation of which is catalyzed by xanthine oxidase and is accompanied by increases in ROS release (Figure 1) [42]. ACH and free radicals produced in the prostate cells via these alternative pathways may promote tumorigenesis [43–46]
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