Wynder E L, Cohen L A, Winters B L
Section of Nutritional Epidemiology, American Health Foundation, New York, NY 10017, USA.
J Am Diet Assoc. 1997 Jul;97(7 Suppl):S5-8. doi: 10.1016/s0002-8223(97)00723-2.
Ecologic comparison of the incidence of cancer (eg, largescale differences between countries in the incidence of breast, prostate, and colon cancer) can be explained best by substantial differences in the intake of dietary fat. Additionally, there is a vast amount of animal and mechanistic data that strongly supports the hypothesis that ditary fat, independent of caloric intake, appears to have a major effect on the incidence and mortality rates for cancer. Yet, results from human case and cohort studies are inconsistent in linking carcinogenesis with fat intake. This is due to several factors. Reported intakes may not reflect previous long-term intakes and may be con-founded by several sources of error, including memory and estimates of portion size. Additionally, ongoing media reports of adverse health effects from high-fat diets may impart a social desirability bias to self-reporting of fat intake. These factors may be significant when investigating the relationship between dietary intake and cancer. Studies have shown considerable error in self-reported dietary data, with under-estimations in energy intake ranging from 3% to 18%. Such a wide range likely is due to differences in dietary assessment methodologies, which highlights the need to continue to develop improved techniques of data collection to relate nutrition better to health outcomes. The Women's Intervention Nutrition Study (WINS) is investigating the effect of dietary fat on the incidence of recurrence and survival in women with early-stage breast cancer. WINS is employing the multiple-pass 24-hour telephone recall system along with enhanced quality control measures to assess dietary intake. This dietary assessment method is particularly applicable when comparing two populations when one population is treated by an extensive dietary intervention.
癌症发病率的生态学比较(例如,各国乳腺癌、前列腺癌和结肠癌发病率的大规模差异)最好用膳食脂肪摄入量的显著差异来解释。此外,大量的动物和机制数据有力地支持了这样一种假说,即膳食脂肪独立于热量摄入,似乎对癌症的发病率和死亡率有重大影响。然而,人类病例和队列研究的结果在将致癌作用与脂肪摄入联系起来方面并不一致。这是由几个因素造成的。报告的摄入量可能无法反映以前的长期摄入量,并且可能受到多种误差来源的混淆,包括记忆和食物分量估计。此外,媒体对高脂饮食不良健康影响的持续报道可能会给脂肪摄入量的自我报告带来社会期望偏差。在研究膳食摄入与癌症之间的关系时,这些因素可能很重要。研究表明,自我报告的饮食数据存在相当大的误差,能量摄入的低估范围在3%至18%之间。如此大的范围可能是由于饮食评估方法的差异,这突出了继续开发改进的数据收集技术以更好地将营养与健康结果联系起来的必要性。妇女干预营养研究(WINS)正在调查膳食脂肪对早期乳腺癌女性复发率和生存率的影响。WINS采用多次24小时电话回忆系统以及强化质量控制措施来评估膳食摄入。当比较两个人群,其中一个人群接受广泛的饮食干预时,这种饮食评估方法特别适用。