***** Five star in terms of being a thought provoking trial - and it was in 1985 !!
Interestingly in rats the risk of developing a mammary tumour were proportionally related to the level of Omega 6 LA intake between 0.5% and 4.4% and after that the risk did not increase.
In the rats the lower the intake of Omega six the lower the risk of tumours developing. Once the level of Omega six reached about 4 1/2% the extra Omega six had little additional effect. Whilst you cannot translate this directly as being applicable in humans there is evidence that tribes on non-western diets are very healthy and relatively free of western conditions on Omega six intakes of under 1%.
The diets in the rats in the trial were
very low in Omega 3. This trial adds to the suggestion that our Omega 6 intake requirement is low and that Omega 6 intake in the absence of Omega 3 at low levels is implicated in the increased risk of cancer. There are other trials that suggest that it is essential to balance the Omega three and six plant-based fats even if the intake of Omega six is very low.
At low intake levels there were even difficulties in inducing cancer, and it was necessary to apply a second dose of a cancer producing agent.The trial is called “Requirement of Essential Fatty Acid for Mammary Tumorigenesis in the Rat” and can be found on FREE the web
http://www.ncbi.nlm.nih.gov/pubmed/3921234.
I have to thank Stephan of the Whole Health blog for finding it.
http://wholehealthsource.blogspot.co...h/label/cancer
I highly recommend his excellent and thought provoking dietary blogs.
ABSTRACT
Requirement of essential fatty acid for mammary tumorigenesis in the rat.
Ip C, Carter CA, Ip MM.
In an attempt to determine the requirement of essential fatty acid for dimethylbenz(a)anthracene-induced mammary tumorigenesis, rats were fed diets containing different levels of linoleate: 0.5, 1.1, 1.7, 2.2, 3.5, 4.4, 8.5, or 11.5%. Each diet contained 20% of fat by weight, with varying amounts of coconut oil and corn oil added to achieve the desired levels of linoleate.
Mammary tumorigenesis was very sensitive to linoleate intake and increased proportionately in the range of 0.5 to 4.4% of dietary linoleate. Regression analysis indicated that a breakpoint occurred at 4.4%, beyond which there was a very poor linear relationship, suggesting the possibility of a plateau. From the intersection of the regression lines in both the upper and lower ranges, the level of linoleate required to elicit the maximal tumorigenic response was estimated to be around 4%. The differences in tumor yield could not be correlated with changes in prostaglandin E concentration in the mammary fat pads of normal animals maintained on similar diets, suggesting that linoleate may act by some other mechanism to stimulate mammary tumorigenesis.
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