Authors: Katz, David L.; Friedman, Rachel S.C.

Title: Nutrition in Clinical Practice: A Comprehensive, Evidence-Based Manual for the Practitioner, 2nd Edition Copyright 2008 Lippincott Williams & Wilkins > Table of Contents > Section II - Nutritional Management in Clinical Practice: Diet, in Sickness and in Health > Chapter 12 - Diet and Cancer Chapter 12 Diet and Cancer Kanker Prostat Terdapat banyak penelitian yang menyatakan diet dan gaya hidup merupakan faktor resiko kanker prostat, tapi masih belum ada bukti yang dapat memastikannya. Studi ekologi dan migrasi menyatakan pola makan negara industri, berkaitan dengan intake tinggi lemak saturasi dan protein dan intake rendah buah dan sayur, berkontribusi meningkatkan resiko kanker prostat. Terdapat bukti yang menyatakan resiko peningkatan resiko berkaitan dengan intake tinggi lemak saturasi dari hewan dan makanan harian. Tetapi, intake lamak bukan resiko prediktif dalam studi case control di inggris, karena tingginya rata-rata intake lemak dan kisaran yang relatif sempit. Berdasarkan studi case control di Swedia, meunjukkan adanya hubungan antara resiko kanker prostat dan diet lemak dengan mengendalikan total energi intake. Adanya perbedaan prostate cancer risk and dietary fat is eliminated by controlling for total energy intake. The discrepancies in the available literature may be interpreted as suggesting that intake of saturated fat or total energy, or both, are among the factors contributing to population risk for prostate cancer but that other important factors remain to be identified to further stratify the risk among members of a population with high or low mean fat and energy intake. As with virtually all other cancers, there is an association between prostate cancer risk and obesity. American Cancer Society data suggest a marked increase in prostate cancer risk with rising BMI (9). A variety of micronutrients have been suggested to protect against prostate cancer, although for most, the evidence is limited. However, as virtually all of the putatively protective nutrients are found in fruits and vegetables, the evidence is more convincing that fruit and vegetable intake may be protective (101). The evidence in support of a specific protective effect of tomatoes and/or their lycopene content raises the possibility that high fruit and vegetable intake is a marker of high tomato intake (98). Of note, whereas the incidence of clinically apparent prostate cancer varies markedly among populations, the incidence of latent cancer appears to be fairly consistent among diverse populations (104,105). This observation suggests that the role of dietary factors may be to inhibit or stimulate the promotion of microscopic tumor foci. Such inhibitory effects have been observed for fatrestricted and soy-supplemented diets in animals (104).

Preliminary evidence has suggested protective effects of vitamins D and E, but further study is required before a basis for recommendations is established (99). Recent data from the ATBC trial suggest that -tocopherol may inhibit the transformation of clinically latent to clinically active prostate cancer. The same study showed a decrease in prostate cancer risk in non-alcohol drinkers receiving -carotene but an increased risk in drinkers (106,107). Like lycopene, -carotene is concentrated in the prostate (108). An inverse association between retinoid intake and prostate cancer risk has been reported fairly consistently. In contrast, intake of retinol has been positively associated with risk in several studies (99). Data from the Health Professionals Follow-up Study suggested an inverse association between prostate cancer risk and intake of lycopene but not other carotenoids (109); a positive association between retinol and cancer risk was not seen. Studies suggesting a protective effect of lycopene generated considerable interest (108), but an association with lycopene was not seen in recent case-control studies (102,110). The largest cohort study to date, involving nearly 30,000 participants, does not support a protective effect of lycopene against prostate cancer (111,112). As tomatoes are the highly predominant source of dietary lycopene, associations observed between lycopene intake and prostate cancer risk may pertain to some other nutrient in tomatoes (109). At this point, data from ongoing randomized controlled trials will be required to establish a role for lycopene in defense against prostate cancer. Uncertainties about dietary factors in the etiology of prostate cancer are highlighted by a case-control study conducted in the United Kingdom, which revealed essentially no association with either fat or carotenoid intake (102). The difference in rates of clinically manifest prostate cancer in the United States and Japan has generated interest in the potential promotional effects of n-6 fatty acids and inhibitory effects of n-3 fatty acids. An in vitro study designed to test this hypothesis had negative results, demonstrating promotional effects of all fats (113).