The traditional diet of Greece and cancer.

[R.B.]

This is about cardiac health and not BC. I post it because it is unusually unequivocal in its statements on the benefits of omega 3s.

It seems to me that anything that assists with cardiac health is good news; it would be nice if they looked to see if omega 3s helped reduce any cardiac implications of Herceptin.

http://www.ncbi.nlm.nih.gov/pubmed/1...ubmed_RVDocSum

Am J Clin Nutr. 2008 Jun;87(6):1991S-6S.
Fish and n-3 fatty acids for the prevention of fatal coronary heart disease and sudden cardiac death.
Mozaffarian D.

Division of Cardiovascular Medicine, Brigham and Women's Hospital, Harvard Medical School, Department of Epidemiology and Nutrition, Harvard School of Public Health, Boston, MA, USA. dmozaffa@hsph.harvard.edu

Large observational studies, randomized clinical trials, and experimental studies have evaluated the effects of fish and n-3 fatty acid consumption on fatal coronary heart disease (CHD) and sudden cardiac death (SCD), clinically defined events that most often share the final common pathway of fatal ventricular arrhythmia. These different study designs, each having complementary strengths and limitations, provide strong concordant evidence that modest consumption of fish or fish oil (1-2 servings/wk of oily fish, or approximately 250 mg/d of EPA+DHA) substantially reduces the risk of CHD death and SCD. Pooled analysis of prospective cohort studies and randomized clinical trials demonstrates the magnitude and dose-response of this effect, with 36% lower risk of CHD death comparing 0 and 250 mg/d of EPA+DHA consumption (P < 0.001), but then little additional benefit with higher intakes. Reductions in risk are even larger in observational studies utilizing tissue biomarkers of n-3 fatty acids that more accurately measure dietary consumption. The concordance of findings from different studies also suggests that effects of fish or fish oil on CHD death and SCD do not vary depending on presence or absence of established CHD. The strength and consistency of the evidence, and the magnitude of this effect are each notable. Because more than one-half of all CHD deaths and two-thirds of SCD occur among individuals without recognized heart disease, modest consumption of fish or fish oil, together with smoking cessation and regular moderate physical activity, should be among the first-line treatments for prevention of CHD death and SCD.

[TSund]

RB,

Thanks for this.

Do I remember you posting some helpful relationship between Omega 3's and Auto-Immune disease?

THX

TRS

[R.B.]

Tsund - thanks for the thanks,

I do not recall doing so, but there may have been a post that was looking at inflammation that also considered auto immune conditions.

Here are two trials that suggest that fish oil / Omegas 3 may assist reduce the risk of auto immune conditions.

RB


http://www.jacn.org/cgi/content/full/21/6/495

Journal of the American College of Nutrition, Vol. 21, No. 6, 495-505 (2002)
Published by the American College of Nutrition
REVIEW
Omega-3 Fatty Acids in Inflammation and Autoimmune Diseases
Artemis P. Simopoulos, MD, FACN

The Center for Genetics, Nutrition and Health, Washington, D.C

Abstract

"There have been a number of clinical trials assessing the benefits of dietary supplementation with fish oils in several inflammatory and autoimmune diseases in humans, including rheumatoid arthritis, Crohn’s disease, ulcerative colitis, psoriasis, lupus erythematosus, multiple sclerosis and migraine headaches. Many of the placebo-controlled trials of fish oil in chronic inflammatory diseases reveal significant benefit, including decreased disease activity and a lowered use of anti-inflammatory drugs."


http://www.ncbi.nlm.nih.gov/pubmed/11802309
Isr Med Assoc J. 2002 Jan;4(1):34-8.Links
n-3 fatty acids and the immune system in autoimmunity.
Ergas D, Eilat E, Mendlovic S, Sthoeger ZM.

Department of Internal Medicine B, Kaplan Medical Center, Rehovot, Israel. ergaz@clalit.org.il

"Therefore, the use of n-3 fatty acids can be recommended to the general healthy population, not only to prevent atherosclerosis but possibly also to reduce the risk of autoimmunity."

[R.B.]

(I re-copied this to this thread as it is significant I suspect)


It all interconnects - what happy coincidences - The post on MS by Bill, and Hopeful of an MMP9 all come together at the same moment in a search for an article on MMP9 omega six and gene expression.

Conclusion Omega 3 suppresses MMP-9 which is a marker of MS and BC

http://www.springerlink.com/content/963788775224p348/

"The treatment with both ω-3 PUFA and fish oil dose-dependently inhibited the LPS-induced production of MMP-9. Our results suggest that a low fat diet supplemented with ω-3 PUFA may become recommended for the well being of MS patients under therapy."

MMP9 has been on my list of interest. I do not know exactly what it is, but saw a trial a long time ago that I will dig out that suggested the omega 3 and 6 significantly change gene expression of MMP9. I have been wondering ever since about MMP 9.



This was posted in articles of interest
http://breastcancersource.com/breast...48_0_0_0.aspx?
2 June 2008
Urine biomarker test confirms breast cancer precursor lesions
MedWire News: Matrix metalloproteinases can be detected in the urine of women with atypical breast hyperplasia and could form the basis for an accurate and convenient test for invasive breast cancer risk, researchers claim.

"Once validated in larger studies, such a test could potentially provide a useful adjunct for breast cancer risk assessment," Marsha Moses (Harvard Medical School, Boston, Massachusetts, USA) and colleagues comment, adding: "The goal of identifying women at high risk of developing breast cancer and providing safe effective risk reduction to this group is compelling."

Matrix metalloproteinases are required for the "angiogenic switch" - an early and critical event in breast cancer growth and progression, Moses et al explain in the journal Cancer Epidemiology, Biomarkers and Prevention.

Matrix metalloproteinase 9 (MMP-9) and a disintegrin and metalloprotease 12 (ADAM 12) are two established serum biomarkers in breast cancer.

[R.B.]

More evidence Omega 6 LA is implicated in BC.

And why COX blockers may have an impact as the block these pathways.

And more PGE2 may = more aromatase = more oestrogen products

More oestrogen would result in more conversion of LA to AA the raw material for this process be enhancing long chain fat conversion.

SO this could be a self fuelling tumour loop where Omega 6 is present in excess and there is no Omega 3 to moderate the process.

RB




http://www.springerlink.com/content/n547j2538p317388/

Xin-Hua Liu1, Jeanne M. Connolly1 and David P. Rose1 Contact Information
(1) Division of Nutrition and Endocrinology, American Health Foundation, Valhalla, New York, USA
(2) Division of Nutrition and Endocrinology, American Health Foundation, 10595 Valhalla, NY, USA

Received: 21 August 1995 Accepted: 27 October 1995

Diets rich in linoleic acid (LA) stimulate the metastasis of MDA-MB-435 human breast cancer cells from the mammary fat pads of nude mice. This omega-6 fatty acid is metabolized to various cyclo-oxygenase and lipoxygenase products, several of which have been previously associated with tumor cell invasion and metastasis. We now report that MDA-MB-435 cells secreted increased levels of prostaglandin E2 (PGE2),

[R.B.]

Striking figures for COX blockers.

DHA is a cox blocker.

It is suggested COX blockers seek to moderate the downstream effect of excess Omega 6.

So balancing Omega 3s and 6s may assist in any COX blocking based strategy.

Please discuss dietary change with your doctor. The posts are only intended to inform debate.



Chemoprevention of Breast Cancer in Rats by Celecoxib, a Cyclooxygenase 2 InhibitorRandall E. Harris2, Galal A. Alshafie, Hussein Abou-Issa and Karen Seibert

School of Public Health [R. E. H., G. A. A., H. A-I.], Comprehensive Cancer Center [R. E. H., H. A-I.], and Department of Surgery [H. A-I.], The Ohio State University College of Medicine, Columbus, Ohio 43210, and Searle Monsanto Research and Development, St. Louis, Missouri 63137 [K. S


Nonsteroidal anti-inflammatory drugs (NSAIDs) have been observed to reduce the relative risk of breast cancer. This prompted our investigation of the chemopreventive potential of celecoxib, a specific cyclooxygenase 2 blocker, against mammary carcinogenesis induced by 7,12-dimethyl-benz(a)anthracene in female Sprague Dawley rats. Treatment with celecoxib was examined and compared to treatment with the general NSAID, ibuprofen, and to a control group receiving only dimethylbenz(a)anthracene. Dietary administration of celecoxib (1500 ppm) produced striking reductions in the incidence, multiplicity, and volume of breast tumors relative to the control group (68%, 86%, and 81%, respectively; P < 0.001). Ibuprofen also produced significant effects, but of lesser magnitude (40%, 52%, and 57%, respectively; P < 0.001). These results help confirm the chemopreventive activity of NSAIDs against breast cancer and provide the first evidence that a cyclooxygenase 2 blocking agent, celecoxib, possesses strong chemopreventive activity against mammary carcinogenesis.

[R.B.]

Cancer therapy for animals

http://www.huntsvillecompounding.com/vet%20cancer.pdf
Gigi Davidson, BSPh, RPh, FSVHP, DICVP
North Carolina State University College of Veterinary Medicine
Raleigh, North Carolina

"Matrix metalloproteinases (especially MMP-2 and MMP-9) are
enzymes that are secreted to degrade the ECM. Any new blood
vessels formed by angiogenesis can migrate only after the ECM is
degraded. MMP-2 and MMP-9 have long been associated with
tumor progression and metastasis.6-8 Although mechanisms of MMP
inhibition remain obscure, n-3 omega fatty acids have been shown
to be very effective MMP inhibitors,"

[R.B.]

Very largely outside my reading but another mechanism by which Omega 3s may reduce the risk of BC.

RB

http://www.ncbi.nlm.nih.gov/pubmed/1...ubmed_RVDocSum

1: Cancer Res. 2008 Apr 15;68(8):2912-9.Click here to read Links
Peroxisome proliferator-activated receptor gamma-mediated up-regulation of syndecan-1 by n-3 fatty acids promotes apoptosis of human breast cancer cells.
Sun H, Berquin IM, Owens RT, O'Flaherty JT, Edwards IJ.

Department of Pathology, Wake Forest University School of Medicine, Winston-Salem, NC 27157, USA.

Diets enriched in n-3 polyunsaturated fatty acids (n-3 PUFA) may protect against breast cancer but biochemical mechanisms are unclear. Our studies showed that the n-3 fatty acid docosahexaenoic acid (DHA) up-regulated syndecan-1 (SDC-1) in human breast cancer cells, and we tested the hypothesis that DHA-mediated up-regulation of SDC-1 induces apoptosis. DHA was delivered to MCF-7 cells by n-3 PUFA-enriched low-density lipoproteins (LDL) or by albumin in the presence or absence of SDC-1 small interfering RNA. The n-3 PUFA induced apoptosis, which was blocked by SDC-1 silencing. We also confirmed that SDC-1 up-regulation and apoptosis promotion by n-3 PUFA was mediated by peroxisome proliferator-activated receptor gamma (PPAR gamma). Using a luciferase gene driven by either a PPAR response element or a DR-1 site present in the SDC-1 promoter, reporter activities were enhanced by n-3 LDL, DHA, and PPAR gamma agonist, whereas activity of a luciferase gene placed downstream of a mutant DR-1 site was unresponsive. Cotransfection with dominant-negative PPAR gamma DNA eliminated the increase in luciferase activity. These data provide strong evidence that SDC-1 is a molecular target of n-3 PUFA in human breast cancer cells through activation of PPAR gamma and that n-3 PUFA-induced apoptosis is mediated by SDC-1. This provides a novel mechanism for the chemopreventive effects of n-3 PUFA in breast cancer.

PMID: 18413760 [PubMed - indexed for MEDLINE]

[R.B.]

WOW - you cannot argue with measured fats in breast tissue, - they do not have momentary memory lapses about what people ate, - they do not respond to very short term dietary changes - they simply and accurately reflect diet.

For me this is powerful evidence that Omega 6 and 3 have a role in the risk of breast cancer occurrence.

The bold and underline are mine.

RB



"We conclude that total n-6 PUFAs may be contributing to the high risk of breast cancer in the United States and that LC n-3 PUFAs, derived from fish oils, may have a protective effect."




Nutr Cancer. 2002;42(2):180-5.

http://www.ncbi.nlm.nih.gov/pubmed/12416257?ordinalpos=1&itool=EntrezSystem2.PEntrez. Pubmed.Pubmed_ResultsPanel.Pubmed_DiscoveryPanel.P ubmed_Discovery_RA&linkpos=2&log$=relatedarticles& logdbfrom=pubmed

Long-chain n-3-to-n-6 polyunsaturated fatty acid ratios in breast adipose tissue from women with and without breast cancer.
Bagga D, Anders KH, Wang HJ, Glaspy JA.

Division of Hematology-Oncology, Department of Medicine, University of California, Los Angeles School of Medicine, Los Angeles, CA 90095, USA.

Animal studies suggest that dietary polyunsaturated fatty acids (PUFAs) of the n-6 class, found in corn and safflower oils, may be precursors of intermediates involved in the development of mammary tumors, whereas long-chain (LC) n-3 PUFAs, found in fish oil, can inhibit these effects. This case-control study was designed to examine the relationship between the PUFA composition of breast adipose tissue and the risk of breast cancer. Using fatty acid levels in breast adipose tissue as a biomarker of past qualitative dietary intake of fatty acids, we examined the hypothesis that breast cancer risk is negatively associated with specific LC n-3 PUFAs (eicosapentaenoic acid and docosahexaenoic acid) and positively associated with n-6 PUFAs (linoleic acid and arachidonic acid). Breast adipose tissue was collected from 73 breast cancer patients and 74 controls with macromastia. The fatty acid levels were determined by gas-liquid chromatography. A logistic regression model was used to obtain odds ratio estimates while adjusting for age. The age-adjusted n-6 PUFA (linoleic acid and arachidonic acid) content was significantly higher in cases than in controls (P = 0.02). There was a trend in the age-adjusted data suggesting that, at a given level of n-6 PUFA, LC n-3 PUFAs (eicosapentaenoic acid and docosahexaenoic acid) may have a protective effect (P = 0.06). A similar inverse relationship was observed with LC n-3-to-n-6 ratio when the data were adjusted for age (P = 0.09). We conclude that total n-6 PUFAs may be contributing to the high risk of breast cancer in the United States and that LC n-3 PUFAs, derived from fish oils, may have a protective effect.

[R.B.]

There are a number of trials with chemo drugs suggesting synergies with long chain Omega 3.

It is something obviously to discuss with your medical adviser before altering your diet.

If you want to search for your particular chemo combinations try entering the drug and DHA or EPA or Omega 3 and see what comes up. You could always take the result along with you to show your advisors. http://www.ncbi.nlm.nih.gov/

Here they are suggesting Omega 3 may effect Her2. [ In an other trial it has been shown Omega 3 and 6 change Her2 gene expression by significant amounts in rat skeletal muscular tissue.]

Trials on other cancers suggest that DHA may increase rates of cell death. In healthy cells long chain omega 3s may be protective and some reports suggest an antioxidant effect - and DHA seems to have a part to play in defective cell kill off. It is very complicated and I only post these views through the thick mist so you understand that DHA is OK for healthy cells - dolphins would be in trouble otherwise (-: with all the fish they eat.


http://www.ncbi.nlm.nih.gov/pubmed/1...ubmed_RVDocSum

J Nutr Biochem. 2008 Jul 3. [Epub ahead of print]Click here to read Links
The potential for treatment with dietary long-chain polyunsaturated n-3 fatty acids during chemotherapy.
Biondo PD, Brindley DN, Sawyer MB, Field CJ.

Department of Agricultural, Food and Nutritional Science, University of Alberta, Edmonton, Alberta, Canada T6G 2P5.

Dietary intake of long-chain omega-3 (or n-3) polyunsaturated fatty acids (PUFA), eicosapentaenoic acid (EPA), and docosahexaenoic acid (DHA) can affect numerous processes in the body, including cardiovascular, neurological and immune functions, as well as cancer. Studies on human cancer cell lines, animal models and preliminary trials with human subjects suggest that administration of EPA and DHA, found naturally in our diet in fatty fish, can alter toxicities and/or activity of many drugs used to treat cancer. Multiple mechanisms are proposed to explain how n-3 PUFA modulate the tumor cell response to chemotherapeutic drugs. n-3 PUFA are readily incorporated into cell membranes and lipid rafts, and their incorporation may affect membrane-associated signaling proteins such as Ras, Akt and Her-2/neu. Due to their high susceptibility to oxidation, it has also been proposed that n-3 PUFA may cause irreversible tumor cell damage through increased lipid peroxidation. n-3 PUFA may increase tumor cell susceptibility to apoptosis by altering expression or function of apoptotic proteins, or by modulating activity of survival-related transcription factors such as nuclear factor-kappaB. Some studies suggest n-3 PUFA may increase drug uptake or even enhance drug activation (e.g., in the case of some nucleoside analogue drugs). Further research is warranted to identify specific mechanisms by which n-3 PUFA increase chemotherapy efficacy and to determine the optimal cellular/membrane levels of n-3 PUFA required to promote these mechanisms, such that these fatty acids may be prescribed as adjuvants to chemotherapy.

[R.B.]

Omega Six The Devils Fat

I have written a book that looks at the impact of EXCESS Omega 6 and lack of Omega 3 on health and behaviour. The subject has become a passion. It will be the diet subject of the next decade. The book is very much less technical than these posts. It is not light reading but has been understood by women from 20 to 80 who have absolutely no technical medical or scientific background. Even self confessed "non readers" have been sufficiently intrigued to spend the time to look at it, once they have dipped into the book.

The material specifically on breast cancer is no where near as comprehensive as this thread, and the book is very much wider, but helps you get a wider perspective of why this is such an important health topic and how it all fits together.

You can read a few pages on Amazon and my web site.

This is a subject that is particularly fundamental to women as women make 10 times as much DHA as men do. DHA is fundamental to women's health and arguably helps define what it is to be a woman.

"GOSH I didn't know that" an expression of genuine surprise and interest, is a generic common reaction of women to some of the material.

The message is simple balance the Omega 3s and 6s. To really appreciate why it is so important you really need to understand a little of why. There are lighter books but this one should leave you in no doubt how important the correct balance of EFAs is to mental and physical health at every level.

WWW.omegasixthedevilsfat.com

http://www.amazon.com/Omega-Six-Devi...5959567&sr=1-1

http://www.amazon.co.uk/Omega-Six-De...5959501&sr=1-1

[AlaskaAngel]

Hi Robert,

I heard this report this weekend on the radio, and thought I'd mention it for consideration:

http://www.npr.org/rss/podcast.php?id=510284

(Look for the July 11, 2008 report)

[R.B.]

Re Talapia - Thanks AA interesting that the subject of excess Omega 6 is making the main stream.

INFLAMMATION - Excess omega 6 and lack of omega 3 promotes inflammation in the body.

It is becoming more and more evident that inflammation is a big factor in the cancer process.

These are some fascinating links that make that point.

http://www3.interscience.wiley.com/j...22663/abstract

ABSTRACT
"In this review I would like to show the evidence that tumor development and progression are accelerated inevitably by inflammation caused from foreign bodies, and that reactive oxygen species derived from inflammatory cells are one of the most important genotoxic mediators to accelerate the process."

http://www3.interscience.wiley.com/j...22662/abstract

ABSTRACT
"Infection and chronic inflammation contribute to about 1 in 4 of all cancer cases. Mediators of the inflammatory response, e.g., cytokines, free radicals, prostaglandins and growth factors, can induce genetic and epigenetic changes including point mutations in tumor suppressor genes, DNA methylation and post-translational modifications, causing alterations in critical pathways responsible for maintaining the normal cellular homeostasis and leading to the development and progression of cancer."

http://www3.interscience.wiley.com/j...22664/abstract

ABSTRACT
" A wide array of chronic inflammatory conditions predispose susceptible cells to neoplastic transformation. In general, the longer the inflammation persists, the higher the risk of cancer. A mutated cell is a sine qua non for carcinogenesis. Inflammatory processes may induce DNA mutations in cells via oxidative/nitrosative stress. "



http://www3.interscience.wiley.com/j...22661/abstract

[R.B.]

http://her2support.org/vbulletin/sho...d=1#post167964

This is a link to Robins fascinating thread on activation of HER2 by a virus (EBV), and inhibition of that virus by long chain Omega 3s.

I thought it was worth re posting here for completeness.

RB

[R.B.]

Complicated but interesting.

Prostaglandins and leukotrienes are products of Omega Six.

It is an interesting suggestion that CLA may inhibit the downstream products of Omega 6. But as ever it is easier to cut down on excess Omega Six and balance with 3s, so avoiding excess Omega 6 products in the first place.

RB



Proliferative responses of normal human mammary and MCF-7 breast cancer cells to linoleic acid, conjugated linoleic acid and eicosanoid synthesis inhibitors in culture

Anticancer Research (Greece) , 1997, 17/1 A (197-203)

Potential mechanisms for the stimulation or inhibition of cell growth by linoleic acid (LA) and conjugated linoleic acid (CLA) were investigated by using eicosanoid linoleic acid (CLA) were investigated by using eicosanoid synthesis inhibitors. Normal human mammary epithelial cells (HMEC) and MCF-7 breast cancer cells were incubated in serum-free medium supplemented with LA or CLA and cyclooxygenase (indomethacin; INDO) or lipoxygenase (nordihydroguaiaretic acid; NDGA) inhibitors. Linoleic acid stimulated the growth and (3H)thymidine incorporation of normal HMEC and MCF-7 cancer cells, while CLA was inhibitory. Supplementation with LA increased intracellular lipid peroxide concentrations in normal HMEC and MCF-7 cancer cells, whereas CLA did not affect lipid peroxide formation. Normal HMEC and MCF-7 cells supplemented with LA and INDO or NDGA resulted in growth inhibition. The treatment of normal HMEC with CLA and INDO or NDGA, and MCF-7 cells with CLA and INDO stimulated cell growth. However, the addition of CLA and NDGA to MCF-7 cells resulted in synergistic growth suppression suggesting that CLA effects were mediated through lipoxygenase inhibition. Although NDGA was more inhibitory of cell growth in the presence of LA or CLA than INDO, growth was associate with both prostaglandin and leukotriene production. Additional studies are warranted to elucidate the mechanism(s)

whereby LA or CLA affect breast cell growth.

[madubois63]

RB - I've mentioned that I am working on helping heal my best friends lymphadema and also have been working very hard on fixing my iron over load in my liver. I grew eating the Mediterranean diet , as both my parents are from Greece. I never had a tv dinner or frozen food until I lived on my own in my 20's. Fast food was unheard of in my household. We only had "spaceburgers" or Jack in the Box the night we decorated the Christmas tree and Chinese in the restaurant on New Years. We fished and clammed all summer and ate our fish in the winter, grew our own veggies and picked our own fruit off the apple. cherry, pear, peach plum and quince trees (native to the Island of Create and my back yard). My mom cooked dandelion, and lentil soups from scratch. The only soup I ever ate from a can was tomato and everything was cooked in olive oil.

I have strayed over the years from a clean diet and paid the price. I have from time to time went back to the old ways, but have strayed many times over. Since becoming sick I have added supplements and herbs to my Mediterranean diet. This time around (the last 2 -3 months) I have really payed attention to everything going in to my body and when (because of my sugar level). The omega's are really important as are the anti-inflammatory herbs and spices. I have scanned your information because I can't always get my head in to reading and retaining information, but I will read it again. Thanks for all the information. This diet has really helped me get my liver functions under control and reducing the iron in my blood.

[R.B.]

Another mechanism by which long chain Omega 3 blocks BC, this time through BRAC1.



1: Oncol Rep. 2007 Apr;17(4):713-9.Click here to read Links
Increased BRCA1 protein in mammary tumours of rats fed marine omega-3 fatty acids.
Jourdan ML, Mahéo K, Barascu A, Goupille C, De Latour MP, Bougnoux P, Rio PG.


INSERM, E 0211; Université François Rabelais; CHU Bretonneau, Tours, F-37000, France.

Any factor affecting BRCA gene regulation may be of interest in the prevention of breast tumourigenesis. We studied the influence of dietary docosahexaenoic acid (DHA), a major omega-3 fatty acid present in marine products, on rat autochthonous mammary tumourigenesis. DHA-supplementation significantly reduced the incidence of tumours (30%, P=0.007) and led to a 60% increase (P=0.02) in BRCA1 protein level. Since DHA influences the product of a major tumour suppressor gene, this finding may contribute to the observation that high-fish consumption reduces the risk of breast cancer.

[Jackie07]

The current issue (Aug. 18/Aug. 25) of US News and World Report has an arrticle - "Making Sense of the Omega Fat Puzzle" by Sarah Baldaug and a health column by Bernadine Healy, former Director of NIH, entitled "From Fish Oil to Medicine".

Dr. Healy says that "... though eating fatty fish is the way to go, refined fish oil supplements with specified doses of EPA (eicosapentaenoic acid) and DHA (docosahexaenoic acid) can make for a more certain prescription, and one that alleviates concerns about fish being contaminated with mercury or PCBs. (Nasty fish burps can be avoided by freezing the gel capsules and taking them at bedtime.) "

[R.B.]

http://www.universityofcalifornia.edu/news/article/7839

Omega-6 fats cause prostate tumors to grow twice as fast
Email this article
Date: 2006-02-01
Contact: Steve Tokar
Phone: (415) 221-4810
Email: steve.tokar@med.va.gov
Omega-6 fatty acids--such as those found in corn oil--caused human prostate tumors in cell culture to grow twice as quickly as tumors to which omega-6 fats had not been added, according to a study conducted at the San Francisco VA Medical Center.

An omega-6 fatty acid known as arachidonic acid turns on a gene signaling pathway that leads directly to tumor growth, according to principal investigator Millie Hughes-Fulford, PhD, director of the Laboratory of Cell Growth at SFVAMC and scientific advisor to the U.S. Under Secretary for Health for the Department of Veterans Affairs.

The results of the study are published in the February 1 issue of Cancer Research.

"After we added omega-6 fatty acids to the growth medium in the dish, and only omega-6, we observed that tumors grew twice as fast as those without omega-6," recounts Hughes-Fulford, who is also an adjunct professor of medicine at the University of California, San Francisco.

"Investigating the reasons for this rapid growth, we discovered that the omega-6 was turning on a dozen inflammatory genes that are known to be important in cancer. We then asked what was turning on those genes, and found that omega-6 fatty acids actually turn on a signal pathway called PI3-kinase that is known to be a key player in cancer," she adds.

Hughes-Fulford says the results are significant because of the high level of omega-6 fatty acids in the modern American diet, mostly in the form of vegetable seed oils such as corn oil-over 25 times the level of beneficial omega-3 fatty acids, which are found in canola oil, fish, and green vegetables. She notes that over the last 60 years, the rate of prostate cancer in the U.S. has increased steadily along with intake of omega-6, suggesting a possible link between diet and prostate cancer.

The study results build on earlier work in which Fulford and her research team found that arachidonic acid stimulated the production of an enzyme known as cPLA-2, which in turn caused a chain of biochemical reactions that led to tumor growth. In the current paper, the researchers have "followed that biochemical cascade upstream to its source," Hughes-Fulford says. "These fatty acids are initiating the signal pathway that begins the whole cascade."

Hughes-Fulford and her fellow researchers also found that if they added a non-steroidal antiflammatory or a PI3K inhibitor to the growth media, interrupting the signal pathway, the genes did not get turned on and increased tumor cell growth did not take place.

Currently, Hughes-Fulford is conducting a study in which research animals are fed diets with different levels of omega-3 and omega-6 fatty acids, "to see how the tumors grow in animals."

Hughes-Fulford says that her study results have directly influenced her own diet. "I'm not a physician, and do not tell people how to eat, but I can tell you what I do in my own home," she says. "I use only canola oil and olive oil. We do not eat deep-fried foods."

Co-authors of the study include Chai-Fei Li, BA, of the Northern California Institute for Research and Education, J.B. Boonyaratanakornkit, BS, of SFVAMC and UCSF, and Sina Sayyah, BA, of NCIRE.

The study was funded by grants from the Department of Veterans Affairs and a grant from NASA that was administered by NCIRE.

UCSF is a leading university that consistently defines health care worldwide by conducting advanced biomedical research, educating graduate students in health care, and providing complex patient care.

[R.B.]

This looks like a fascinating and informative paper. I have not paid to view it but part is available at the lower link.

Definitely worth at least a skim if you have the time.

It emphasises the importance of the Omega 3:6 ratio in breast cancer risk, and in one place suggests a need for a ration of around 1:1 or 1:2 Omega 3 :6.

http://www.ncbi.nlm.nih.gov/pubmed/16145262

http://books.google.co.uk/books?hl=e...HJLU#PPA147,M1