Prostate Cancer Growth Increases with Omega-6 Diet, but Slows with Omega-3.
Bottomline: A cleverly designed study shows that high dietary omega-6 fat triggers tumor growth, in an animal model of prostate cancer, while dietary omega-3 fat attenuates. Neoplasia (2009):11(7):692-699
Background: Prostate cancer is one of the leading causes of death among men in the USA. Previous studies implicate the imbalance of dietary omega-6 and omega-3 fats, in part, for the high occurrence of prostate cancer.
Recent data show that two key enzymes are increased in prostate tumor tissues, compared to normal tissues. One of these enzymes is 15-lipoxygenase-1 (15-LOX-1), which prefers linoleic acid, rather than arachidonic acid (both of which are omega-6 polyunsaturated fatty acids.) The compound created from the union of linoleic acid and 15-LOX-1, contributes to the initiation and development of prostate cancer.
The other enzyme that increases in prostate cancer is COX-2, which acts on arachidonic acid to create PGE-2, which is also implicated in prostate cancer (and other cancers as well, see China Study Shows Dietary Arachidonic Acid Ups Risk for Colorectal Cancer.) A recent study, demonstrated that prostate cancer cell growth was inhibited, with the combination of DHA and celecoxib (a medication which is a specific COX-2 inhibitor).
Enter the EPA factor. When the above two enzymes (5-LOX-1 and COX-2), joins with EPA, it creates anti-inflammatory and anti-tumorogenic compounds. Taken together, there is a double beneficial effect with increased dietary EPA:
Study: An animal model of prostate cancer was used. The mice were injected with prostate cancer-promoting cells and divided into three-isocaloric diets: the control diet, high linoleic acid (omega-6) diet and high omega-3 diet. (Note, because of cost constraints, the researchers used the omega-3 fatty acid, stearidonic acid, which is the precursor to EPA.)
This was a 28-week dietary study, with a crossover-design at week 23. At week 23, the high omega-6 diet group was switched over to the high omega-3 diet, and visa versa, the omega-3 fed mice were crossed-over to the omega-6 diet. At week 28 tumors were evaluated for growth, fatty acids, enzyme activities, apoptosis and proliferation.
Results: Tumors from the high omega-6 diet group had the most rapid growth. Yet, when this omega-6 fed group was switched to the omega-3 diet, there was a dramatic decrease in tumor growth. When the omega-3 diet group was switched to the omega-6 diet, the tumors grew more aggressively.
The omega-6 and omega-3 fatty acid composition of red blood cells and tumor cells, reflected the diet, and modulated accordingly. The tumors from the high omega-6 group, had a higher ratio of omega-6:omega-3 fat, nearly 7-fold, compared to the control group. Similarly, the tumors from the omega-3 fed group, had a 4-fold decrease in the ratio, compared to the control.
Conclusion: Dietary omega-6 and omega-3 fatty acids, effects cell composition, which in turn, influence the activities of enzymes, 15-LO-1 and COX, which effect prostate cancer growth. When EPA competes with arachidonic and linoleic acid, for COX and 15-LO-1 enzymes, respectively, it slows prostate cancer growth by creating tumor inhibiting compounds.
Quote: "Importantly, these results further corroborate that SDA (and EPA) does not inhibit either 15-LO-1 or COX, and tumor growth reflects the substrate competition of omega-3 and omega-6 fatty acids."
Link to Full Text Study:
Kelavkar U et al. Prostate tumor growth can be modulated by dietarily targeting the 15-lipoxygenase-1 and cyclooxygenase-2 enzymes.
Neoplasia (2009):11(7):692-699.
Background: Prostate cancer is one of the leading causes of death among men in the USA. Previous studies implicate the imbalance of dietary omega-6 and omega-3 fats, in part, for the high occurrence of prostate cancer.
Recent data show that two key enzymes are increased in prostate tumor tissues, compared to normal tissues. One of these enzymes is 15-lipoxygenase-1 (15-LOX-1), which prefers linoleic acid, rather than arachidonic acid (both of which are omega-6 polyunsaturated fatty acids.) The compound created from the union of linoleic acid and 15-LOX-1, contributes to the initiation and development of prostate cancer.
The other enzyme that increases in prostate cancer is COX-2, which acts on arachidonic acid to create PGE-2, which is also implicated in prostate cancer (and other cancers as well, see China Study Shows Dietary Arachidonic Acid Ups Risk for Colorectal Cancer.)
Enter the EPA factor. When the above two enzymes (5-LOX-1 and COX-2), joins with EPA, it creates anti-inflammatory and anti-tumorogenic compounds. Taken together, there is a double beneficial effect with increased dietary EPA:
- Increases anti-tumorogenic compounds
- Decreases the availability of these enzymes to make tumor promoting compounds from omega-6 fat.
Study: An animal model of prostate cancer was used. The mice were injected with prostate cancer-promoting cells and divided into three-isocaloric diets: the control diet, high linoleic acid (omega-6) diet and high omega-3 diet. (Note, because of cost constraints, the researchers used the omega-3 fatty acid, stearidonic acid, which is the precursor to EPA.)
This was a 28-week dietary study, with a crossover-design at week 23. At week 23, the high omega-6 diet group was switched over to the high omega-3 diet, and visa versa, the omega-3 fed mice were crossed-over to the omega-6 diet. At week 28 tumors were evaluated for growth, fatty acids, enzyme activities, apoptosis and proliferation.
Results: Tumors from the high omega-6 diet group had the most rapid growth. Yet, when this omega-6 fed group was switched to the omega-3 diet, there was a dramatic decrease in tumor growth. When the omega-3 diet group was switched to the omega-6 diet, the tumors grew more aggressively.
The omega-6 and omega-3 fatty acid composition of red blood cells and tumor cells, reflected the diet, and modulated accordingly. The tumors from the high omega-6 group, had a higher ratio of omega-6:omega-3 fat, nearly 7-fold, compared to the control group. Similarly, the tumors from the omega-3 fed group, had a 4-fold decrease in the ratio, compared to the control.
Conclusion: Dietary omega-6 and omega-3 fatty acids, effects cell composition, which in turn, influence the activities of enzymes, 15-LO-1 and COX, which effect prostate cancer growth. When EPA competes with arachidonic and linoleic acid, for COX and 15-LO-1 enzymes, respectively, it slows prostate cancer growth by creating tumor inhibiting compounds.
Quote: "Importantly, these results further corroborate that SDA (and EPA) does not inhibit either 15-LO-1 or COX, and tumor growth reflects the substrate competition of omega-3 and omega-6 fatty acids."
Link to Full Text Study:
Kelavkar U et al. Prostate tumor growth can be modulated by dietarily targeting the 15-lipoxygenase-1 and cyclooxygenase-2 enzymes.
Neoplasia (2009):11(7):692-699.
www.EvelynTribole.com
Posted by Evelyn Tribole MSRD at September 27, 2009 7:12 PM 
Categories: Arachidonic Acid, Linoleic Acid, LOX, Cancer, omega-6/omega-3 Ratio, 2009 Studies, polyunsaturated fatty acids, Cox, Nutrition, EPA, Biomarkers, Full Text Studies-FREE
Categories: Arachidonic Acid, Linoleic Acid, LOX, Cancer, omega-6/omega-3 Ratio, 2009 Studies, polyunsaturated fatty acids, Cox, Nutrition, EPA, Biomarkers, Full Text Studies-FREE
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