Virtamo Jarmo, Pietinen Pirjo, Huttunen Jussi K, Korhonen Pasi, Malila Nea, Virtanen Mikko J, Albanes Demetrius, Taylor Phil R, Albert Paul
National Public Health Institute, Helsinki, Finland.
JAMA. 2003 Jul 23;290(4):476-85. doi: 10.1001/jama.290.4.476.
In the Finnish Alpha-Tocopherol, Beta-Carotene Cancer Prevention (ATBC) Study, alpha-tocopherol supplementation decreased prostate cancer incidence, whereas beta-carotene increased the risk of lung cancer and total mortality. Postintervention follow-up provides information regarding duration of the intervention effects and may reveal potential late effects of these antioxidants.
To analyze postintervention effects of alpha-tocopherol and beta-carotene on cancer incidence and total and cause-specific mortality.
DESIGN, SETTING, AND PARTICIPANTS: Postintervention follow-up assessment of cancer incidence and cause-specific mortality (6 years [May 1, 1993-April 30, 1999]) and total mortality (8 years [May 1, 1993-April 30, 2001]) of 25 563 men. In the ATBC Study, 29 133 male smokers aged 50 to 69 years received alpha-tocopherol (50 mg), beta-carotene (20 mg), both agents, or placebo daily for 5 to 8 years. End point information was obtained from the Finnish Cancer Registry and the Register of Causes of Death. Cancer cases were confirmed through medical record review.
Site-specific cancer incidence and total and cause-specific mortality and calendar time-specific risk for lung cancer incidence and total mortality.
Overall posttrial relative risk (RR) for lung cancer incidence (n = 1037) was 1.06 (95% confidence interval [CI], 0.94-1.20) among recipients of beta-carotene compared with nonrecipients. For prostate cancer incidence (n = 672), the RR was 0.88 (95% CI, 0.76-1.03) for participants receiving alpha-tocopherol compared with nonrecipients. No late preventive effects on other cancers were observed for either supplement. There were 7261 individuals who died by April 30, 2001, during the posttrial follow-up period; the RR was 1.01 (95% CI, 0.96-1.05) for alpha-tocopherol recipients vs nonrecipients and 1.07 (95% CI, 1.02-1.12) for beta-carotene recipients vs nonrecipients. Regarding duration of intervention effects and potential late effects, the excess risk for beta-carotene recipients was no longer evident 4 to 6 years after ending the intervention and was primarily due to cardiovascular diseases.
The beneficial and adverse effects of supplemental alpha-tocopherol and beta-carotene disappeared during postintervention follow-up. The preventive effects of alpha-tocopherol on prostate cancer require confirmation in other trials. Smokers should avoid beta-carotene supplementation.
在芬兰的α-生育酚、β-胡萝卜素癌症预防（ATBC）研究中，补充α-生育酚可降低前列腺癌发病率，而补充β-胡萝卜素会增加肺癌风险和总死亡率。干预后的随访提供了有关干预效果持续时间的信息，并可能揭示这些抗氧化剂的潜在晚期影响。
分析α-生育酚和β-胡萝卜素干预后对癌症发病率、总死亡率和特定病因死亡率的影响。
设计、地点和参与者：对25563名男性进行干预后癌症发病率和特定病因死亡率（6年[1993年5月1日至1999年4月30日]）以及总死亡率（8年[1993年5月1日至2001年4月30日]）的随访评估。在ATBC研究中，29133名年龄在50至69岁的男性吸烟者每天接受α-生育酚（50毫克）、β-胡萝卜素（20毫克）、两种药物或安慰剂，持续5至8年。终点信息来自芬兰癌症登记处和死亡原因登记处。癌症病例通过病历审查得到证实。
特定部位癌症发病率、总死亡率和特定病因死亡率以及肺癌发病率和总死亡率的日历时间特定风险。
与未接受β-胡萝卜素的人相比，接受β-胡萝卜素的人肺癌发病率（n = 1037）的总体试验后相对风险（RR）为1.06（95%置信区间[CI]，0.94 - 1.20）。对于前列腺癌发病率（n = 672），与未接受α-生育酚的参与者相比，接受α-生育酚的参与者的RR为0.88（95% CI，0.76 - 1.03）。两种补充剂均未观察到对其他癌症的晚期预防作用。在试验后随访期间，到2001年4月30日有7261人死亡；接受α-生育酚者与未接受者相比的RR为1.01（95% CI，0.96 - 1.05），接受β-胡萝卜素者与未接受者相比的RR为1.07（95% CI，1.02 - 1.12）。关于干预效果的持续时间和潜在的晚期影响，β-胡萝卜素接受者的额外风险在干预结束4至6年后不再明显，主要是由于心血管疾病。
补充α-生育酚和β-胡萝卜素的有益和不良影响在干预后随访期间消失。α-生育酚对前列腺癌的预防作用需要在其他试验中得到证实。吸烟者应避免补充β-胡萝卜素。
