Supplemental and dietary vitamin E, β-carotene, and vitamin C intakes and prostate cancer risk

Supplemental and dietary vitamin E, β-carotene, and vitamin C intakes and prostate cancer risk
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DOI:
10.1093/jnci/djj050
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发表时间:
2006-02-15
影响因子:
10.3
通讯作者:
Peters, U
Peters, U
中科院分区:
医学1区
文献类型:
--
作者:
Kirsh, VA;Hayes, RB;Peters, U

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背景维生素E、β-胡萝卜素和维生素C是微量营养素抗氧化剂,可保护细胞免受前列腺癌发生过程中的氧化损伤。在单独的试验中,补充维生素E与吸烟者前列腺癌风险降低相关,补充β-胡萝卜素与基线血浆β-胡萝卜素水平低的男性前列腺癌风险降低相关。研究方法:我们在前列腺癌、肺癌、结直肠癌和卵巢癌筛查试验的筛查组中评估了从食物和补充剂中摄入这些微量营养素抗氧化剂与男性患前列腺癌风险之间的关联。在基线时,试验参与者完成了一份137项食物频率问卷,其中包括12种补充剂的详细问题。使用考克斯比例风险模型估计相对风险(RR)和95%置信区间(Cls)。所有统计检验均为双侧检验。结果:我们在29361名男性中发现了1338例前列腺癌,随访时间为8年。总的来说,前列腺癌风险与饮食或补充维生素E、β-胡萝卜素或维生素C的摄入量之间没有关联。然而,在当前和最近(即,在前10年内)吸烟者,降低晚期前列腺癌的风险(即,Gleason评分>= 7或III或IV期)与剂量增加相关(>400 IU/天与无的RR = 0.291,95%)CI = 0.12至0.68; P趋势= 0.01)和持续时间(使用≥ 10年与不使用的RR = 0.30,950%,CI = 0.09至0.96; P趋势= 0.01)补充维生素E的使用。补充β-胡萝卜素摄入量至少为2000 μ g/天与低(低于中位数4129 μ g/天)饮食β-胡萝卜素摄入量的男性前列腺癌风险降低相关(RR = 0.52,95% CI = 0.33至0.81)。在吸烟者中,年龄调整后的晚期前列腺癌发病率在未补充维生素E的人群中为492/10万人年,在补充维生素E超过400 IU/天的人群中为153/10万人年,在补充维生素E 10年或更长时间的人群中为157/10万人年。在饮食β-胡萝卜素摄入量低的男性中,未补充β-胡萝卜素的人群中,年龄调整后的前列腺癌发病率为1122/10万人年,而补充β-胡萝卜素至少2000微克/天的人群中,年龄调整后的前列腺癌发病率为623/10万人年。结论:我们的研究结果并没有提供强有力的支持,为预防前列腺癌的人群广泛实施高剂量的抗氧化剂补充。然而,男性吸烟者补充维生素E和饮食中β-胡萝卜素摄入量低的男性补充β-胡萝卜素与降低这种疾病的风险有关。
Background. Vitamin E, beta-carotene, and vitamin C are micronutrient antioxidants that protect cells from oxidative damage involved in prostate carcinogenesis. In separate trials, supplemental vitamin E was associated with a decreased risk of prostate cancer among smokers and supplemental beta-carotene was associated with a decreased risk of prostate cancer among men with low baseline plasma beta-carotene levels. Methods: We evaluated the association between intake of these micronutrient antioxidants from foods and supplements and the risk of prostate cancer among men in the screening arm of the Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial. At baseline, trial participants completed a 137-item food frequency questionnaire that included detailed questions on 12 individual supplements. Cox proportional hazards models were used to estimate relative risks (RRs) and 95% confidence intervals (Cls). All statistical tests were two-sided. Results: We identified 1338 cases of prostate cancer among 29361 men during tip to 8 years of follow-up. Overall, there was no association between prostate cancer risk and dietary or supplemental intake of vitamin E, beta-carotene, or vitamin C. However, among current and recent (i.e., within the previous 10 years) smokers, decreasing risks of advanced prostate cancer (i.e., Gleason score >= 7 or stage III or IV) were associated with increasing dose (RR for >400 IU/day versus none = 0.291,95%) Cl = 0.12 to 0.68; P-trend =.01) and duration (RR for >= 10 years of use versus none = 0.30, 950%, CI = 0.09 to 0.96; P-trend =.01) of supplemental vitamin E use. Supplemental beta-carotene intake at a dose level of at least 2000 mu g/day was associated with decreased prostate cancer risk in men with low (below the median of 4129 mu g/day) dietary beta-carotene intake (RR = 0.52, 95% Cl = 0.33 to 0.81). Among smokers, the age-adjusted rate of advanced prostate cancer was 492 per 100000 person-years in those who did not take supplemental vitamin E, 153 per 100000 person-years in those who took more than 400 IU/day of supplemental vitamin E, and 157 per 100000 person-years in those who took supplemental vitamin E for 10 or more years. Among men with low dietary beta-carotene intake, the age-adjusted rate of prostate cancer was 1122 per 100000 person-years in those who did not take supplemental beta-carotene, and 623 per 100000 person-years in those who took at least 2000 mu g/day of supplemental beta-carotene. Conclusions: Our results do not provide strong support for population-wide implementation of high-dose antioxidant supplementation for the prevention of prostate cancer. However, vitamin E supplementation in male smokers and beta-carotene supplementation in men with low dietary beta-carotene intakes were associated with reduced risk of this disease.