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

[Guest guest]

> 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?

Hi Rodney. I think it's them; the shorter the PSA doubling time, the faster

the cancer is proliferating - bad ju-ju.

Al

[Guest guest]

> 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?

Hi Rodney. I think it's them; the shorter the PSA doubling time, the faster

the cancer is proliferating - bad ju-ju.

Al

[Guest guest]

Yes, a slower doubling time is considered good because the rate of cancer increase effect on PSA is less. In patients with fast rate the object is to slow the growth, measured by PSA.

I'm still wondering about SDA. If the EPA is not being made, SDA may not be there, and substituting EPA may not be adequate.

Maybe tricky wording, because they conclude to use EPA.

Don't have the full text.

Regards.

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

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.>> 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]

Yes, a slower doubling time is considered good because the rate of cancer increase effect on PSA is less. In patients with fast rate the object is to slow the growth, measured by PSA.

I'm still wondering about SDA. If the EPA is not being made, SDA may not be there, and substituting EPA may not be adequate.

Maybe tricky wording, because they conclude to use EPA.

Don't have the full text.

Regards.

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

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.>> 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>