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Influence of dietary factors on actinically-induced skin cancer.

机译:饮食因素对光化性皮肤癌的影响。

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The first indication that high dietary fat intake could influence the development of ultraviolet (UV) radiation-induced skin cancer in experimental animals was reported in 1939. In the 1980s a series of animal studies showed that a high level of dietary fat intake markedly shortened the time between UV exposure and tumor appearance and increased the number of tumors that developed. Further, high levels of dietary fat affected skin cancer development at the promotional stage of UV-carcinogenesis, i.e., after the cancer causing dose of UV had been delivered. Perhaps more important, switching from a high-fat to a low-fat diet immediately after delivery of the UV-initiating dose negated the exacerbating effect of high fat intake. The latter finding suggested that dietary modification, even after a cancer-causing exposure to UV, might represent a potentially important intervention strategy in the prevention of non-melanoma skin cancer (NMSC) and provided the rationale for undertaking a dietary intervention trial. One hundred and fifteen skin cancer patients completed the 2-year clinical trial on the effect of a low-fat diet on occurrence of actinic keratosis (AK) and NMSC. Patients were randomly assigned to either continue their usual diet (control group, NI) or to adopt a diet with 20% of total caloric intake as fat (diet intervention group, DI). All patients were examined at 4-month intervals for new AK and NMSC. At baseline, the mean percent of caloric intake as fat was 40+/-4% in the NI group and 39+/-3% in the DI group. After 4 months of dietary therapy, the percent calories as fat had decreased to 21+/-7% in the DI group. The percent of calories as fat in the NI group did not drop below 37% during the study period. The cumulative number of new AK per patient from months 4 through 24 was 11.6+/-17 in the NI group and 3.2+/-6 in the DI group (P < 0.001). Numbers of new NMSC were analyzed in 8-month periods. There were no significant changes in NMSC occurrence in the NI group. However, NMSC occurrence in the DI group declined significantly (P < 0.02) in the last 8-month period. Patients in the DI group also had significantly (P < 0.01) fewer NMSC in the last 8-month period than did patients in the NI group (0.02 versus 0.26). Practical dietary advice, with respect to reduction of percent of calories as fat, could make an important contribution to the prevention and management of AK and NMSC.
机译:1939年首次报道了高饮食脂肪摄入可能影响实验动物中紫外线(UV)辐射诱发的皮肤癌的发展。1980年代的一系列动物研究表明,高饮食脂肪摄入显着缩短了动物体内的脂肪摄入。紫外线暴露与肿瘤出现之间的时间间隔,并增加了所形成肿瘤的数量。此外,在紫外线致癌的促进阶段,即在已经引起引起紫外线剂量的癌症之后,高水平的饮食脂肪会影响皮肤癌的发展。也许更重要的是,在递送紫外线引发剂量后立即从高脂饮食转向低脂饮食,却抵消了高脂肪摄入的加剧作用。后者的发现表明,即使在引起癌症的紫外线照射后,饮食调整也可能代表了预防非黑素瘤皮肤癌(NMSC)的潜在重要干预策略,并为进行饮食干预试验提供了依据。 115位皮肤癌患者完成了为期2年的临床研究,研究涉及低脂饮食对光化性角化病(AK)和NMSC发生的影响。随机分配患者继续常规饮食(对照组,NI)或采用总热量摄入量的20%作为脂肪的饮食(饮食干预组,DI)。所有患者均每4个月检查一次新的AK和NMSC。基线时,NI组的热量摄入平均百分数为脂肪,为40 +/- 4%,DI组为39 +/- 3%。饮食治疗4个月后,DI组的脂肪卡路里百分比降低至21 +/- 7%。在研究期间,NI组中作为脂肪的卡路里百分比未降至37%以下。 NI组每位患者从第4个月到第24个月的新AK累积数量为11.6 +/- 17,DI组为3.2 +/- 6(P <0.001)。在8个月内分析了新的NMSC的数量。 NI组中NMSC的发生没有明显变化。但是,DI组的NMSC发生率在最近8个月中显着下降(P <0.02)。 DI组的患者在最近8个月中的NMSC也明显少于NI组(0.02对0.26)(P <0.01)。关于减少卡路里(脂肪)百分比的实用饮食建议可以对AK和NMSC的预防和管理做出重要贡献。

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