Research Results and Status as of September 2004
HEAL research summarized in the following graphs reveals that commonly purchased vitamin E (alpha tocopheryl-acetate) increased trout hepatoma several fold in the presence of small amounts of aflatoxin. Vitamin E-succinate in contrast markedly reduced hepatoma incidence.
Since aflatoxin is responsible for many cases of human liver cancer, especially in 3rd world countries and also in the United States, the type of vitamin E used will be expected to affect human cancer incidence.
The results of this work suggest other keys to our understanding of the cancer problem.
Elevated vit. E-acetate (groups 8, 21 & 34) increased carcinomas 2 to 3 fold. In contrast vit. E-succinate (groups 29-33) prevented liver carcinomas (versus group 2). All these diets had the same amount of aflatoxin.
After six weeks on the respective diets, livers of those fish fed elevated Vitamin E-acetate were markedly de-pigmented, hypertrophic and rigid. The above data is of fish on the diets 6 & 9 months respectively, which showed the physical damage caused by vitamin E-acetate.
Fish fed diets with aflatoxin and elevated Vitamin E-acetate (even groups 7, 11, 13 etc.) had 3 to 4 times the cellular carcinoma rate as the aflatoxin fed control, group # 2. Comparison with groups 1,19 & 20 (no aflatoxin) show that vit. E-Ac is a promoter but only rarely induced cancer in the absence of aflatoxin.
Histopathology assessment of cellular carcinomas compared to visible tumors on whole liver surfaces from fish fed equal amounts of aflatoxin (except for its absence in groups 1 and 19).
The succinic acid ester of vitamin E greatly reduces or eliminates aflatoxin induced trout hepatomas. This mimics the protection reported for human cell line breast, prostrate, colon cancers and murine leukemia with this compound.
In stark contrast the acetate ester of vitamin E markedly increases hepatoma incidence.
These have far reaching implications respectively for prevention or promotion of cancer in humans.