Abstract

The promoting effect of dietary fat in experimental carcinogenesis was first shown by Watson and Mellanby in 1930 (1). They found that raising the usual 3% fat content of their diet to 12.5–25.0% by addition of butter increased the incidence of skin tumors in coal tar-treated mice by 68%. Several years later Baumann et al. (2) demonstrated that increasing dietary fat (Crisco) from 5 to 25% increased the incidence of skin tumors initiated in mice by ultraviolet irradiation or benzo (a) pyrene (BP) painting. In order to ascertain which fraction of fat was responsible for the increase in tumor formation Lavik and Baumann (3) treated mice topically with methylcholanthrene (MC) and fed 15% hydrogenated vegetable oil, 15% ethyl laurate, 5% glycerol or the unsaponifiable matter obtained from vegetable oil. After 4.5 months tumor yields were 60%, 63%, 47% and 35%, respectively. In the same system heated fat was considerably more tumorigenic (70% incidence at 6 months) then oxidized fat (38%) or irradeated fat (40%). The intact fat (hydrogenated vegetable oil) led to 31% incidence of skin tumors. Their work led Miller et al. (4) to compare the effects of different fats on the carcinogenicity of p-dimethylaminobenzene (DAB) using diets containing 5% fat they compared the effects of corn oil (CO), coconut oil (CNO), hydrogenated coconut oil (HCNO), trilaurin, CO-HCNO 4:1 and CO-HCNO 1:4. The greatest incidence of hepatomas was seen in rats fed CO or CO-HCNO 4:1. A later study (5) compared the effects on DAB-induced hepatomas of 5% corn or olive oil and 20% corn oil, Crisco or lard. Incidence of induced hepatomas at 4 months was: 5% corn oil, 73%; 5% olive oil, 13%; 20% corn oil, 100%; 20% Crisco, 47%; and 20% lard, 60%.

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