Fish oils: rich in EPA (Eicosapentaenoic Acid... Omega 3 Oil)
Flax oil: rich in ALA (Alpha-Linolenic Acid.... Omega 3 Oil)... body converts into EPA
Nuts: GLA (Gamma Linoleic Acid.... Omega 6 Oil)
(For more detailed information, please visit ISM’s searchable database: Nutraceutical Search.)
· The metabolism of essential polyunsaturated fatty acids (PUFA) appears to be one of the critical targets in the complex metabolic stages that lead to, or are associated with cancer. EFAs (EPA and DHA acid) may be recommended as supplementation and in addition to current therapy during cancer treatment.
o P R Health Sci J. 2004 Jun; 23(2): 107-13.
· Omega-3 (n-3) fatty acids (FA) have been proposed to confer tumor-inhibitory properties. In vivo, dietary FA are delivered to tumor cells by two main routes: low-density lipoproteins (LDL) and albumin complexes.
o Clin Cancer Res. 2004 Dec 15; 10(24): 8275-83.
Oral administration of a supplement rich in omega-3 fatty acids for 5 d before surgery may improve not only preoperative nutritional status but also preoperative and postoperative inflammatory and immune responses in patients who have cancer.
o Nutrition. 2005 Jun; 21(6): 639-49.
· Anti-cachectic: EFAs prevent & reverse wasting syndrome.
o Ross, Curr.Opin. Coin. Nutr. Metab. Care. (1999)vol 2, no. 3, p 219
EFAs induce apoptosis (suicide) in cells.o Hardman, (2002) J. Nutr. Vol 132, no. 11, p.3508s
· EFAs slow metastasis.
o Woutersen, Mutat. Res. (1999) vol 443, no. 1, p 11.
EFAs impair tumour angiogenesis.o Rose, (2000) nutr. Cancer, vol 37, no 2, p 119
· 21 patients with failed medical treatment & untreatable malignacies with GLA experienced weight gain & reduction in tumour size.
o Vander Merwe, Brit. J. Clin. Prac. (1987) vol 41, p 907
· Dietary supplementation with EPA decreases natural killer cell activity in healthy subjects aged >55 y.
o Thies, Am J Clin Nutr (2001);73:539-48
· There may be inhibition of specific enzymes that play an important role in determining membrane phospholipid fatty acid composition.
o Eur J Clin Nutr. 1993 Apr; 47(4): 260-7.
In several epidemiological studies, a phytoestrogen-rich diet containing lignans and isoflavones is associated with reduced breast cancer risk. In postmenopausal mammary cancer xenograft model, flaxseed (FS), a rich source of plant lignans, reduced breast cancer growth. Flax seed may have tumour growth attenating effect.o Int J Cancer. 2006 Mar 23.
GLA given to breast cancer patients (w. Tamoxifen therapy) showed 400% increase in complete response compared to control of just Tamoxifen.o Kenny, Int. J. of Cancer (2000) vol 85, p643
· A diet rich in omega-3 polyunsaturated fatty acids (PUFAs) could reduce the risk of colorectal cancer by 85 per cent.
o Kiyonori Kuriki, Journal Cancer Epidemiology, Biomarkers & Prevention 2006 Vol. 15, pp.1791–1798
Five or more servings of fish a week was associated with a 40 per cent reduction in colorectal cancer risk, compared to men who ate fish less than once a week. The relative risk of eating fish 2-5 times a week was 20 per cent lower, and 13 per cent lower among participants who ate fish less than twice a week. The underlying mechanism was not studied by the researchers, but they suggested that the omega-3 fatty acids content of the fish inhibit the cyclooxygenase-2 (COX-2) enzyme that plays a role in inflammatory responses and has been linked to cancer development.o Megan Phillips, Harvard School of Public Health and Brigham and Women's Hospital, American Association for Cancer Research’s Frontiers in Cancer Prevention Research meeting. October 2006
Data from 1 million participants in the European Prospective Investigation into Cancer and Nutrition (EPIC) trial indicates that people eating less than 14g of fish a day were 40 per cent more likely to develop colorectal cancer than those eating more than 50g per day.o Journal of the National Cancer Institute (Vol. 97, no 12)
Consumption of fish rich in n-3 polyunsaturated fatty acids (PUFAs), such as docosahexaenoic acid, is suggested to reduce colorectal cancer risk through inhibition of the arachidonic acid (AA) cascade related to tumorigenesis and cell proliferation.o Kiyonori Kuriki, Cancer Epidemiology Biomarkers & Prevention Vol. 15, 1791-1798, October 2006
The erythrocyte saturation index of fatty acids was lower in patients with primary and recurrent colorectal cancer compared with control subjectso Dis Colon Rectum. 1990 Dec; 33(12): 1026-30.
· There was a significantly reduced omega-3/omega-6 polyunsaturated fatty acid ratio in prostate cancer patients. The pronounced elevations in prostatic tissue in cancer patients highlight a possible role of this fatty acid in neoplastic processes.
o Prostaglandins Leukot Essent Fatty Acids. 2002 May-Jun; 66(5-6): 467-77.
There is increasing evidence that EFAs may have a role to play in the aetiology of some types of cancer although their precise mode of action is unknown.o Br J Cancer. 1991 Dec; 64(6): 1157-60.
Red cell membrane Fatty Acid saturation correlates well with radiological and biochemical markers of advanced prostatic carcinoma and may be used as a marker to assess progress and response to treatment.o Br J Urol. 1990 Mar; 65(3): 268-70.
There were consistent trends for increasing prostate cancer risk with higher levels of trans-fatty acids.o Cancer Epidemiology Biomarkers & Prevention April 2005; (14): 988-992.
This study reviews the effects of omega-3 fatty acids, eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), and the omega-6 fatty acid, arachidonic acid (AA), on the spread of human prostate cancer cell lines. The researchers found that a metabolite of AA, prostaglandin E2, helped the spread of the prostate cancer cells to bone marrow cells. However, when EPA and DHA were present at just half the concentration of the omega-6 fatty acid, this spread of cancer cells was stopped. Some tumours develop slowly in the prostate without producing symptoms and sometimes when symptoms do develop, it is because the cancer has already spread. Eating a diet with the right balance of omega 3 and omega 6 fats may well help to keep prostate cancer within the prostate gland.”o Clarke, British Journal of Cancer March 2006 (doi: 10.1038/sj.bjc.6603030)