Here are 2 original studies claiming that EFAD is a promoting condition for tumorigenesis:
Prostaglandins Leukot Essent Fatty Acids. 1997 Mar;56(3):239-44.
Dietary deficiency or enrichment of essential fatty acids modulates tumorigenesis in the whole body of cobalt-60-irradiated mice.
Eynard AR, Manzur T, Moyano A, Quiroga P, Muñoz S, Silva SM.
Instituto Biologia Celular (FCM-UNC), CONICET, Cordoba, Argentina.
The effect of dietary polyunsaturated fatty acids (PUFAs) on whole body-induced tumorigenesis was assayed in mice fed on essential fatty acid sufficient (EFAS) or essential fatty acid deficient (EFAD) diets following cobalt-60 irradiation. Four groups of mice were maintained, one on a control stock diet and three on experimental diets: a) without added fat (fat free, FF); b) containing 5% olein (O), rich in n-9; and c) containing 5% corn oil, rich in n-6 EFA (CO). Only mice fed on FF or O diets showed clinical and biochemical signs of EFAD. Total incidence of tumors showed an increase in FF (P < 0.02) and O (P < 0.03) mice. Tumors developed mostly in the liver in each of the EFAD groups (P < 0.001). Slight promoting activity on lung tumorigenesis was recorded in the CO group when this parameter was compared in EFAD and EFA sufficient mice. It may be concluded that, when a tumor initiator injures the body as a whole, EFAD, achieved either through a fat-free or an oleic-supplemented diet, behaves as a general promoting condition for tumorigenesis. The borderline tumorigenic effect of n-6 corn oil on the lungs suggests that this effect, when present, is target specific.
PMID: 9089806
Nutrition. 1999 Mar;15(3):208-12.
Differential effects of dietary Oenothera, Zizyphus mistol, and corn oils, and essential fatty acid deficiency on the progression of a murine mammary gland adenocarcinoma.
Muñoz SE, Piegari M, Guzmán CA, Eynard AR.
I Cátedra de Histología, FCM, Córdoba, Argentina.
The modulating effect of dietary enrichment in mistol seed oil (MO) containing 25% of alpha-linolenic acid (ALA), evening primrose oil (EPO) enriched in gamma-linolenic acid (GLA) and corn oil (CO) as sources of omega-6 and omega-9 fatty acids on the growth parameters of one transplantable mammary tumor were compared. Mice fed on different lipid formulae were inoculated with a mammary gland adenocarcinoma and different growth development tumor parameters were recorded. Results showed that corn oil feeding slowed down most of the tumor growth parameters, as did the EPO diet. MO also showed antitumor activity. Olein feeding, which induces an essential fatty acid deficiency (EFAD), increased the incidence and the multiplicity of metastases when compared with the controls. It may be concluded that a diet enriched in omega-6 fatty acids did not behave as a tumor promoter in this mammary gland tumor model. The antitumor activities of EPO and MO are corroborated in present experiments, suggesting that both oils may be of value in nutritional approaches of mammary gland tumor therapies. In addition, present data add further experimental proof about the proposed protumorigenic proneness induced by the EFAD state.
PMID: 10198915
and the following study reveals that primose oil fed rats have have 21% fewer carcinomas than the corn oil fed rats despite of having significantly higher AA levels:
Lipids. 1988 Oct;23(10):948-54.
Eicosanoid synthesis in 7,12-dimethylbenz(a)anthracene-induced mammary carcinomas in Sprague-Dawley rats fed primrose oil, menhaden oil or corn oil diet.
Abou-el-Ela SH, Prasse KW, Carroll R, Wade AE, Dharwadkar S, Bunce OR.
Department of Pharmacology and Toxicology, College of Pharmacy, University of Georgia, Athens 30602.
The comparative effects of high-fat diets (20%, w/w) on eicosanoid synthesis during mammary tumor promotion in 7,12-dimethylbenz(a)anthracene (DMBA)-induced rats were studied using diets containing 20% primrose oil (PO), 20% menhaden oil (MO) or 20% corn oil (CO). Sprague-Dawley rats fed the PO or MO diet had 21% of 24% fewer adenocarcinomas, respectively, than rats fed the CO diet. Histologically (i.e., mitotic figures, inflammatory cell infiltration and necrosis), the CO-fed rats exhibited the highest frequency of changes within tumors. Plasma fatty acid composition was significantly altered by diet, reflecting the composition of the oils which were being fed. Only the plasma of PO-fed rats contained detectable levels of gamma-linolenic acid (GLA). Arachidonic acid (AA) levels were significantly higher (p less than 0.05) in PO-fed than in CO- or MO-fed rats. MO-fed rats had significantly higher levels of plasma palmitic acid, while palmitoleic, eicosapentaenoic (EPA) and docosahexaenoic (DHA) acids were detected only in MO-fed rats. As expected, linoleic acid (LA) and AA levels were lower (p less than 0.05) in the MO-fed rats than in PO- or CO-fed groups. The plasma of the CO-fed rats contained significantly higher levels of oleic acid. Eicosanoid synthesis in mammary carcinomas of rats fed the 20%-fat diets was 2-10 times higher than in mammary fat pads of control rats.(ABSTRACT TRUNCATED AT 250 WORDS)
PMID: 3143882
does this mean that AA is protective against cancers?? |
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