Another example which misleads people to consuming Omega-3s and avoiding saturated fat:
Cancer Res. 2008 Apr 15;68(8):3066-73.
Effect of low-fat diet on development of prostate cancer and Akt phosphorylation in the Hi-Myc transgenic mouse model.
Kobayashi N, Barnard RJ, Said J, Hong-Gonzalez J, Corman DM, Ku M, Doan NB, Gui D, Elashoff D, Cohen P, Aronson WJ.
Department of Urology, School of Medicine, University of California, Los Angeles, CA 90095-1738, USA.
This study evaluated the effect of dietary fat on prostate cancer development by using the Hi-Myc mouse transgenic prostate cancer model. Hi-Myc mice develop murine prostatic intraepithelial neoplasia (mPIN) as early as 2 to 4 weeks and invasive adenocarcinoma between 6 and 9 months due to the overexpression of human c-Myc in the mouse prostate. Three-week-old male Hi-Myc mice were placed on high-fat (HF; 42% Kcal) or low-fat (LF; 12% Kcal) diets, and equal caloric intake was maintained until euthanasia at 7 months. The number of mice that developed invasive adenocarcinoma at 7 months was 27% less in the LF diet group (12/28) compared with the HF diet group (23/33, P < 0.05). Epithelial cells in mPIN lesions in the LF group had a significantly lower proliferative index compared with epithelial cells in the HF group (21.7% versus 28.9%, P < 0.05). During the mPIN phase of carcinogenesis (4 months), the LF group had higher serum insulin-like growth factor (IGF) binding protein-1 levels (21.0 +/- 8.9 ng/mL versus 3.2 +/- 0.8 ng/mL, P < 0.05) relative to the HF group. Akt (Ser(473)) phosphorylation, Akt kinase activity, and phosphorylation of downstream targets of Akt in prostates were significantly reduced in the LF diet group compared with the HF group. We conclude that dietary fat reduction delays transition from mPIN to invasive cancer in this Myc-driven transgenic mouse model, possibly through suppression of the IGF-Akt pathway and decreased proliferation of mPIN epithelial cells.
PMID: 18413778
The comment by an "expert" Dr. Gabe Mirkin:
Fewer Omega-6's May Reduce Cancer Risk
Researchers at UCLA show that reducing intake of corn
oils helps to prevent prostate cancer in mice (Cancer Research,
April 15, 2008). Corn oil and other vegetable oils are extremely
rich sources of omega-6 fatty acids.
Fats are classified by their chemical structure into
omega-3s, omega-6s, and omega-9s. Omega-6s cause your body to
produce prostaglandins that turn on your immunity to cause
inflammation, while omega-3s turn down your immunity to reduce
inflammation.
Your immunity is supposed to be good for you. When a
germ enters your body, your immunity produces white blood cells
and proteins called antibodies that attack and kill the germ.
After that germ is gone, your immunity is supposed to stop making
so many immune cells and proteins. If it remains active, your
immunity attacks your own body to damage tissue and increase
risk for heart attacks, certain cancers, and diabetes; it can
also worsen existing diseases such as some types of dementia,
asthma or psoriasis.
For more than 2 million years, humans have eaten diets
that have a ratio of omega-6s to omega-3s of about two to one.
However, over the last 100 years, humans have added extracted
vegetable oils to other foods that they eat and increased the
ratio to 12 to one and perhaps as high as 20 to one. This increase
in the ratio of omega-6s to omega-3s is a cause of inflammation.
The increase in omega-6's has come primarily from
vegetable oils that are added to baked, fried and other prepared
foods. Omega-3s oils are relatively unstable so they are not
found in most prepared foods.
Good food sources of omega-3's include seafood and
beans, whole grains, nuts and other seeds. We do not know if
changing the ratio of omega-6s to omega-3s will help to prevent
cancers in humans, but several studies show that they appear to
both prevent and slow cancers in animals. |
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