Prostate Tumor Growth and Recurrence Can Be Modulated by the omega-6:omega-3

[Guest guest]

This suggests LA increases risk, ALA decreases. At least it agrees with the biochem - effects on eicosanoids. Disagrees with the one article blaming ALA.

Suggests EPA/DHA.

"Our results provide evidence that .............the omega-3 fatty acid SDA [precursor of eicosapentaenoic acid (EPA)] promotes apoptosis" suggests the ALA is also important.

Regards.

Neoplasia. 2006 Feb;8(2):112-24.

Prostate Tumor Growth and Recurrence Can Be Modulated by the omega-6:omega-3 Ratio in Diet: Athymic Mouse Xenograft Model Simulating Radical Prostatectomy.Kelavkar UP, Hutzley J, Dhir R, Kim P, KG, McHugh K.Department of Urology and Cancer Institute, University of Pittsburgh, Pittsburgh, PA, USA, Email: kelavkarup@....Evidence indicates that a diet rich in omega (omega)-6 polyunsaturated fatty acids (PUFAs) [e.g., linoleic acid (LA)] increases prostate cancer (PCa) risk, whereas a diet rich in omega-3 decreases risk. Precisely how these PUFAs affect disease development remains unclear. So we examined the roles that PUFAs play in PCa, and we determined if increased omega-3 consumption can impede tumor growth. ..........

Our results provide evidence that prostate tumors can be modulated by the manipulation of omega-6:omega-3 ratios through diet and that the omega-3 fatty acid SDA [precursor of eicosapentaenoic acid (EPA)] promotes apoptosis and decreases proliferation in cancer cells, causing decreased PSA doubling time, compared to omega-6 LA fatty acid, likely by competing with the enzymes of LA and AA pathways, namely, 15-LO-1 and cyclooxygenases (COXs). Thus, EPA and DHA (major components of fish oil) could potentially be promising dietary intervention agents in PCa prevention aimed at 15-LO-1 and COX-2 as molecular targets. These observations also provide clues as to its mechanisms of action.PMID: 16611404

[Guest guest]

Hi JW:

Is a " decreased doubling time " supposed to be good or bad? If my PSA

was to double in less time (one year instead of two years, say) I

would have thought that was bad. But they seem to see it as good?

Is it me that is confused? Or them?

Rodney.

--- In , " jwwright " <jwwright@...>

wrote:

>

> This suggests LA increases risk, ALA decreases. At least it agrees

with the biochem - effects on eicosanoids. Disagrees with the one

article blaming ALA.

> Suggests EPA/DHA.

> " Our results provide evidence that .............the omega-3 fatty

acid SDA [precursor of eicosapentaenoic acid (EPA)] promotes

apoptosis " suggests the ALA is also important.

> Regards.

>

> Neoplasia. 2006 Feb;8(2):112-24.

>

>

> Prostate Tumor Growth and Recurrence Can Be Modulated by the omega-

6:omega-3 Ratio in Diet: Athymic Mouse Xenograft Model Simulating

Radical Prostatectomy.

>

> Kelavkar UP, Hutzley J, Dhir R, Kim P, KG, McHugh K.

>

> Department of Urology and Cancer Institute, University of

Pittsburgh, Pittsburgh, PA, USA, Email: kelavkarup@...

>

> Evidence indicates that a diet rich in omega (omega)-6

polyunsaturated fatty acids (PUFAs) [e.g., linoleic acid (LA)]

increases prostate cancer (PCa) risk, whereas a diet rich in omega-3

decreases risk. Precisely how these PUFAs affect disease development

remains unclear. So we examined the roles that PUFAs play in PCa, and

we determined if increased omega-3 consumption can impede tumor

growth. ..........

>

> Our results provide evidence that prostate tumors can be modulated

by the manipulation of omega-6:omega-3 ratios through diet and that

the omega-3 fatty acid SDA [precursor of eicosapentaenoic acid (EPA)]

promotes apoptosis and decreases proliferation in cancer cells,

causing decreased PSA doubling time, compared to omega-6 LA fatty

acid, likely by competing with the enzymes of LA and AA pathways,

namely, 15-LO-1 and cyclooxygenases (COXs). Thus, EPA and DHA (major

components of fish oil) could potentially be promising dietary

intervention agents in PCa prevention aimed at 15-LO-1 and COX-2 as

molecular targets. These observations also provide clues as to its

mechanisms of action.

>

> PMID: 16611404

>

[Guest guest]

Hi JW:

Is a " decreased doubling time " supposed to be good or bad? If my PSA

was to double in less time (one year instead of two years, say) I

would have thought that was bad. But they seem to see it as good?

Is it me that is confused? Or them?

Rodney.

--- In , " jwwright " <jwwright@...>

wrote:

>

> This suggests LA increases risk, ALA decreases. At least it agrees

with the biochem - effects on eicosanoids. Disagrees with the one

article blaming ALA.

> Suggests EPA/DHA.

> " Our results provide evidence that .............the omega-3 fatty

acid SDA [precursor of eicosapentaenoic acid (EPA)] promotes

apoptosis " suggests the ALA is also important.

> Regards.

>

> Neoplasia. 2006 Feb;8(2):112-24.

>

>

> Prostate Tumor Growth and Recurrence Can Be Modulated by the omega-

6:omega-3 Ratio in Diet: Athymic Mouse Xenograft Model Simulating

Radical Prostatectomy.

>

> Kelavkar UP, Hutzley J, Dhir R, Kim P, KG, McHugh K.

>

> Department of Urology and Cancer Institute, University of

Pittsburgh, Pittsburgh, PA, USA, Email: kelavkarup@...

>

> Evidence indicates that a diet rich in omega (omega)-6

polyunsaturated fatty acids (PUFAs) [e.g., linoleic acid (LA)]

increases prostate cancer (PCa) risk, whereas a diet rich in omega-3

decreases risk. Precisely how these PUFAs affect disease development

remains unclear. So we examined the roles that PUFAs play in PCa, and

we determined if increased omega-3 consumption can impede tumor

growth. ..........

>

> Our results provide evidence that prostate tumors can be modulated

by the manipulation of omega-6:omega-3 ratios through diet and that

the omega-3 fatty acid SDA [precursor of eicosapentaenoic acid (EPA)]

promotes apoptosis and decreases proliferation in cancer cells,

causing decreased PSA doubling time, compared to omega-6 LA fatty

acid, likely by competing with the enzymes of LA and AA pathways,

namely, 15-LO-1 and cyclooxygenases (COXs). Thus, EPA and DHA (major

components of fish oil) could potentially be promising dietary

intervention agents in PCa prevention aimed at 15-LO-1 and COX-2 as

molecular targets. These observations also provide clues as to its

mechanisms of action.

>

> PMID: 16611404

>