Yesterday, I reported to you how a change in the rules has changed diagnosing prostate cancers.
Because of these changes, many prostate cancers are being ignored, or misclassified, or not diagnosed.
Today I want to show you one of the most beneficial ways that you can reduce your chances of getting prostate cancer.
Remember that prostate cancer is the most common form of cancer, with at least 14% of men diagnosed in their lifetime.
Autopsies of men who died of random causes show that the number may be much higher.
At least one-third of these autopsies are shown to have prostate cancer that they didn’t even know about.
But it certainly beneficial to not get prostate cancer, and here’s what today’s study shows us.
What researchers did was that they induced human prostate cancer in mice.
Then they put these mice on various diets with different fat consumption.
These diets ranged from under 3% of calories from fat to 40% of calories from fat.
Then the researchers monitored the mice to see about the spread of the prostate cancer.
They also checked the PSA levels in the blood of these mice.
PSA is Prostate Specific Antigen.
It’s a protein that is found in seminal fluid in small quantities.
Elevated levels of PSA can indicate a number of issues — including prostate cancer.
The findings of the study were surprising!
Tumor growth rates, final tumor weights, and ratios of final tumor weights to animal weights were substantially greater in groups that continued to receive a high fat diet.
Mice that received the low-fat diet lived longer — their cancer spread more slowly, and their PSA levels were much lower.
The lowest PSA levels were in the low-fat mice, the mice eating a diet of less than 3% of the calories from fat.
Researchers did not notice any other difference in the weight or testosterone levels in the mice fed different levels of fat.
The ONLY difference that they noticed was the lowered threat of the tumor, and that correlated very well with the PSA levels.
Low PSA levels were more common in the low-fat mice.
And the low-fat mice had much lower tumor growth.
The type of fat is also very important to preventing tumors.
In another study, they fed various types of oils to mice that had been given breast tumors.
They tried corn oil, fish oil, and saturated fat such as dairy fat and other types of fat.
Experiments with 10 different fats and oils fed at the 20% level indicated that unsaturated fats enhance the yield of adenocarcinomas more than saturated fats.
This study is evidence that PUFAs increase the chances of getting tumors and cancer.
In the first study that we just talked about (prostate cancer), they fed these mice bad quality fat.
The diets were high in PUFAs.
They didn’t pay attention to the type of fat is much as they did in the breast tumor study.
I think that a high-fat diet is probably safer if it’s saturated fat.
There is ample evidence and theory showing that PUFAs, unsaturated fats, increase the chances of getting cancer, and increase the rate of tumor growth.
What should you do now?
You might want to consider eliminating PUFAs from your diet.
You might even consider lowering all the fat levels in your diet.
This is not good news for people who believe in a high-fat low-carb diet.
That type of diet seems to promote the growth of tumors and cancer.
It’s even worse if the fat that they do consume is high in PUFAs.
Many low carb dieters eat a lot of PUFAs including nuts, seeds, whole grains, and vegetable oil.
These are all high in PUFAs.
So people following this sort of diet are probably promoting tumor growth and increasing the chances of getting cancer.
Citations
SEER Stat Fact Sheets: Prostate Cancer
http://seer.cancer.gov/statfacts/html/prost.html
Decreased Growth of Established Human Prostate LNCaP Tumors in Nude Mice Fed a Low-Fat Diet
http://jnci.oxfordjournals.org/content/87/19/1456.abstract?ijkey=c532693eaad7bf5aa5d0517dc11d127bcacc8c31&keytype2=tf_ipsecsha
Effects of level and type of dietary fat on incidence of mammary tumors induced in female sprague-dawley rats by 7,12-dimethylbenz(α) anthracene
http://link.springer.com/article/10.1007/BF02531379
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