Quoted message said:There's a lot more thinking you're going to want to do. Start with
Bruce Fif'es book, Saturated fat may save your life. There are a few
problems with it, but it's good for those who need an introduction to
the key issues, not the nonsense you hear from the talking heads on TV.
Instead of reading "a book [someguy] wrote" I'd heavily suggest to stick to
published studies from peer-reviewed journals.
Like:
Int J Oncol. 2005 Mar;26(3):785-92. Links
A combination of docosahexaenoic acid and celecoxib prevents prostate cancer
cell growth in vitro and is associated with modulation of nuclear
factor-kappaB, and steroid hormone receptors.
Narayanan NK, Narayanan BA, Reddy BS.
Department of Environmental Medicine, New York University School of
Medicine, Tuxedo, NY 10987, USA. [email hidden].
Epidemiological studies have provided evidence that high intake of saturated
fat and/or animal fat increases the risk of prostate cancer, but on the
other hand, diets rich in omega-3 polyunsaturated fatty acids (n-3 PUFAs),
present in fish oils were found to reduce the risk. There are indications of
an increased expression of immunoreactive PPARgamma in prostatic
intraepithelial neoplasia (PIN) and prostate cancer, suggesting that
PPARgamma ligands may exert their own potent anti-proliferative effect
against prostate cancer. The experimental evidence for the role of
cyclooxygenase-2 (COX-2) in prostate carcinogenesis is well established
through several investigations. It clearly suggests the need for development
of strategies to inhibit COX-2 mediated prostate carcinogenesis. However,
administration of high doses of COX-2 inhibitors, such as celecoxib, over
longer periods may not be devoid of side effects. We assessed the efficacy
of DHA and celecoxib individually and in combination at low doses in three
prostate cancer cell lines (LNCaP, DU145 and PC-3) measuring cell growth
inhibition and apoptosis, and on the levels of expression of COX-2, nuclear
factor-kappaB (NF-kappaBp65), and nuclear receptors, such as PPARgamma and
retinoid X receptors (RXR), all of which presumably participate in prostate
carcinogenesis. A 48-h incubation of prostate cancer cells with 5 microM
each of DHA or celecoxib induced cell growth inhibition and apoptosis, and
altered the expression of the above molecular parameters. Interestingly, the
modulation of these cellular and molecular parameters was more pronounced in
cells treated with low doses of DHA and celecoxib (2.5 microM each) in
combination than in cells treated with the higher doses of individual
agents. In conclusion, the present study demonstrates for the first time
that a combination of lower doses of the n-3 PUFA, and DHA with the
selective COX-2 inhibitor celecoxib effectively modulates the above cellular
and molecular parameters that are relevant to prostate cancer. This raises
the intriguing prospect that the use of low doses of a COX-2 inhibitor in
combination with an n-3 PUFA could be a highly promising strategy for
prostate cancer chemoprevention while minimizing undesired side effects.
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Br J Cancer. 2005 Feb 01; [Epub ahead of print] Related Articles,
Links
Specific fatty acid intake and the risk of pancreatic cancer in Canada.
Nkondjock A, Krewski D, Johnson KC, Ghadirian P.
[1] 1Epidemiology Research Unit, Research Centre, Centre hospitalier de
l'Universite de Montreal (CHUM)-Hotel-Dieu, Montreal, QC, Canada [2]
2McLaughlin Centre for Population Health Risk Assessment, Institute of
Population Health, University of Ottawa, Ottawa, ON, Canada.
The possible association of specific fatty acid (FA) intake and pancreatic
cancer risk was investigated in a population-based case-control study of 462
histologically confirmed cases and 4721 frequency-matched controls in eight
Canadian provinces between 1994 and 1997. Dietary intake was assessed by
means of a self-administered food frequency questionnaire. Unconditional
logistic regression was used to assess associations between dietary FAs and
pancreatic cancer risk. After adjustment for age, province, body mass index,
smoking, educational attainment, fat and total energy intake, statistically
significant inverse associations were observed between pancreatic cancer
risk and palmitate (odds ratios (ORs)=0.73; 95% confidence intervals (CIs)
0.56-0.96; P-trend=0.02), stearate (OR=0.70; 95% CI 0.51-0.94;
P-trend=0.04), oleate (OR=0.75; 95% CI 0.55-1.02; P-trend=0.04), saturated
FAs (OR=0.67; 95% CI 0.50-0.91; P-trend=0.01), and monounsaturated FAs
(OR=0.72; 95% CI 0.53-0.98; P-trend=0.02), when comparing the highest
quartile of intake to the lowest. Significant interactions were detected
between body mass index and both saturated and monounsaturated FAs, with a
markedly reduced risk associated with intake of stearate (OR=0.36; 95% CI
0.18-0.70; P-trend=0.001), oleate (OR=0.36; 95% CI 0.19-0.72;
P-trend=0.002), saturated FAs (OR=0.35; 95% CI 0.18-0.67; P-trend=0.002),
and monounsaturated FAs (OR=0.32; 95% CI 0.16-0.63; P-trend<0.0001) among
subjects who are obese. The results suggest that substituting
polyunsaturated FAs with saturated or monounsaturated FAs may reduce
pancreatic cancer risk, independently of total energy intake, particularly
among obese subjects.British Journal of Cancer advance online publication, 1
February 2005; doi:10.1038/sj.bjc.6602380 www.bjcancer.com.
