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Total Calories and Dietary Fat
High calorie intake has ben associated with increased cancer risk, independent of high fat contnt. In one review of data from 100 animal experiments, both high calorie and high fat diets independently increased spontaneous mammary tumor incidence. The effect of a high fat diet was two-thirds the magnitude of a high calorie effect. Other invstigators have reported that small reductions in calorie consumption (eg 12%) substantially reduce mammary tumor development in animals, whereas large reductions of fat are required to reach the same effect.
One mechanism by which high calorie diets may increase cancer incidence is by increasing metabolism, and therefore increasing free radical generation. NOTE: Long-term calorie restriction is associated with an inhibition in lipid peroxidation in animals.
The amount and type of dietary fat consumed may affect cancer growth through numerous mechanisms. High-fat diets, in particular those rich in Omega-6 fatty Acids may promote cancer growth. Mechanisms include increasing sex hormone bioavailability, decreasing the immune response, increasing production of PGE2, increasing membrane fluidity and increasing the production of free radicals. On the other hand diets rich in Omega-3 fatty acids, in particular EPA, may inhibit cancer growth. This may occur by markedly decreasing membrane fluidity, markedly decreasing free radical damage, increasing PGE3 production, decreasing PGE2 production, reducing platelet aggregation, decreasing the production of angiogenic factors and decreasing bodily weakness.
Other Macronutrients
Modification of other macronutrients may inhibit the growth of some cancers. These measures include reducing total calorie intake, reducing sugar intake, increasing fibre intake, and reducing the intake of animal products.
Micronutrients
Dietary micronutrients such as minerals and vitamins appear to play a significant role in preventing the development of various cancers. The study of the effects of micronutrients on cancer is hampered by the variability of micronutrients in foods, the variability of human diets, the difficulty of long-term dietary recall, and the modest effect that these micronutrients generally produce.
(Editor's Note: While the importance of minerals in the human diet has long been recognised, the effectiveness of mineral supplementation has always been limited by the micron sizes of mineral particles formerly available in supplement form. Powdered minerals and colloidal minerals have a bioavailability of no more than 3% at most due to their large particle size which prevented absorption by the cells. This has severely hampered their effectiveness. A recent development has been the production of angstrom-sized minerals, 100% available to the body's cells and 100% effective in assisting the body to prevent and fight diseases, including cancers of all kinds).
The most important vitamins are possibly vitamins A, C E, B6 and folic acid. High doses of vitamin A necessary to cause differentiation of cancer cells are also toxic to the liver. Vitamin C in large doses appears to lengthen the lifespan and wellbeing of the patient while reducing pain. Vitamin E plays an important anticarcinogenic role in scavnging free radicals, but this is more preventive function than therapy.
Vitamin B6 Vitamin B6 deficiency may be involved in carcinogenesis, since it is required for DNA repair. In established cancers, however B6 supplementation may be detrimental. A number of animal and in vitro studies have indicated that B6 may increase the proliferation of various cancer cell lines and B6 deficiency can actually inhibit proliferation. Several human tumor xenografts in mice exhibited increased growth with B6 administration and reduced growth with B6 deficiency. In a study of 248 patients with ovarian epithelial cancer, administration of B6 significantly reduced the neurotoxicity of cisplatin and hexamethylmlamine, presumably by facilitating the repair of drug-induced DNA lesions. However it adversely affected the survival of patients given these chemotherapy drugs.
Folic Acid
Folic Acid is a cofactor in numrous biochemical processes in the body, and shares many of the same functions as vitamin B12. One of these functions is protein synthesis. In particular folic acid (folate) is required in the formation of thymidylate, which is the rate-limiting step in DNA synthesis. Therefore, deficiency of folate inhibits DNA synthesis and may also stop the rapid proliferation of cells in a fast-growing tumor. The chemotherapy drugs methotrexate and aminopterin, are synthetic analogs of folate that inhibit tumor cell growth by interfering with folic acid and thus DNA synthesis. These drugs are most effective against fast-growing tumors, since cells of these tumors are sites of rapid DNA synthesis.
Although folate inhibitors are used to treat cancer, adequate folic acid is necessary to prevent some cancers. Low folic acid intake, or low erythrocyte levels, are associated with increased risk of developing colorectal and cervical cancers. Folic acid may reduce the risk of cervical cancer by inhibiting the incorporation of human papilloma virus genes into fragile chromosomal sites in affected cells. Low erythrocyte levels are a risk factor for abnormal cytological smears in both benign atypia and more advanced lesions, and folic acid supplementation has been used very effectively to treat precancerous changes in the cervix.
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