Low Fat Dietary Guide To Aid In The Management Of Skin Cancer
Why Diet?
The
first indication that dietary fat could influence the development of
UV-induced skin cancer came in 1939. The researchers reported that when
experimental animals were fed a diet that contained a high fat
level, the time for cancer development after exposure to UV rays was
significantly shortened. Although there was some interest in this area of
investigation in the early 1940’s, this research lead was not actively
pursued for another 45 years. In the 1980’s American and Australian
researchers confirmed, in closely-controlled nutritional studies,
that the level and nature of dietary fat could exert profound
influence on the course of experimental UV-induced skin cancer.
Subsequently, this influence of dietary fat was shown to occur principally
after a cancer causing dose of UV had already been administered.
Further, by switching from a high- fat to a low-fat diet shortly after
administration of the cancer causing dose of UV, the influence of high-fat
intake in provoking the appearance of skin cancers could be
significantly diminished. It is known that among persons who have
had at least one skin cancer, 28% are at risk to have another
within the following two years. Thus, the experimental findings
suggested that by adopting a low-fat diet, skin cancer patients might reduce
their risk for developing new skin cancers and provided the basis for
undertaking a clinical trial to test this hypothesis.
Skin cancer patients were assigned to one of two groups in the
study. In the first group no changes in eating habits were
introduced, allowing patients to continue to consume about 36-40%
of their total calorie intake as fat. Patients in the other group
were instructed in adopting low-fat eating habits with the
goal of reducing the percent of calories from fat to around 20%. The
potential benefit for this low-fat intervention became apparent early in the
clinical study. A clear and significant difference in the number of
actinic keratoses (pre-malignant skin lesions that result from
excessive sun exposure and that sometimes develop directly into
skin cancer) occurred between patients who continued to consume
diets high in fat and those who adopted low- fat eating habits. Patients
consuming high levels of fat were found to be at nearly five- times
greater risk of developing one or more actinic keratosis during the
2-year period of the study than patients in the low-fat
“intervention” group. Further, after 115 patients had completed the
study, a similar, dramatic effect on non-melanoma skin cancer (both
basal and squamous cell carcinoma) occurrence was observed.
Overall, the methods for controlling fat intake permitted
considerable flexibility in food choices since foods with little or no fat
were emphasized, although higher-fat foods could be included as long
as one did not go beyond the recommended fat gram goal (the grams of
fat a patient could consume which would not exceed 20% of his or her
total daily calorie intake from fat). Thus, a singular strategy of reducing
fat intake, with the goal of 20% of calories from fat, could be an
effective aid in the management and prevention of non- melanoma
skin cancer and pre-malignant actinic keratosis. The question now
remains, “How do I follow such a diet?”