The traditional diet of Greece and cancer.

[R.B.]

Synergistic effects of garlic and Omega 3 EPA

eicosapentaenoic acid = EPA
linoleic acid = common plant based Omega 6

Anticancer Agents Med Chem. 2011 Jan 26. [Epub ahead of print]
Anticancer Effects of Garlic and Garlic-derived Compounds for Breast Cancer Control.

Tsubura A, Lai YC, Kuwata M, Uehara N, Yoshizawa K.

Department of Pathology II, Kansai Medical University, Moriguchi, Osaka 570-8506, Japan. tsubura@takii.kmu.ac.jp.
Abstract

Garlic and garlic-derived compounds reduce the development of mammary cancer in animals and suppress the growth of human breast cancer cells in culture. Oil-soluble compounds derived from garlic, such as diallyl disulfide (DADS), are more effective than water-soluble compounds in suppressing breast cancer. Mechanisms of action include the activation of metabolizing enzymes that detoxify carcinogens, the suppression of DNA adduct formation, the inhibition of the production of reactive oxygen species, the regulation of cell-cycle arrest and the induction of apoptosis. Selenium-enriched garlic or organoselenium compounds provide more potent protection against mammary carcinogenesis in rats and greater inhibition of breast cancer cells in culture than natural garlic or the respective organosulfur analogues. DADS synergizes the effect of eicosapentaenoic acid, a breast cancer suppressor, and antagonizes the effect of linoleic acid, a breast cancer enhancer. Moreover, garlic extract reduces the side effects caused by anti-cancer agents. Thus, garlic and garlic-derived compounds are promising candidates for breast cancer control.

[R.B.]

FADS 1 and 2 play a role in the creation of long chain polyunsaturated fats. There are genetic variants of FADS that make our ability to convert plant fats to long chain fats more or less efficient.

Those with less efficient conversion may have a greater need for food like fish which supply the long chain fats like DHA and EPA ready made.

Our ability to make EPA and DHA has a wide range of health and functional impacts, including the amount of EPA and DHA in breast milk.




Exp Biol Med (Maywood). 2010 Jul;235(7):785-95.
Genetic variants in the metabolism of omega-6 and omega-3 fatty acids: their role in the determination of nutritional requirements and chronic disease risk.

Simopoulos AP.

The Center for Genetics, Nutrition and Health, 2001 S Street NW, Washington, DC 20009, USA. cgnh@bellatlantic.net
Abstract

The tissue composition of polyunsaturated fatty acids is important to health and depends on both dietary intake and metabolism controlled by genetic polymorphisms that should be taken into consideration in the determination of nutritional requirements. Therefore at the same dietary intake of linoleic acid (LA) and alpha-linolenic acid (ALA), their respective health effects may differ due to genetic differences in metabolism. Delta-5 and delta-6 desaturases, FADS1 and FADS2, respectively, influence the serum, plasma and membrane phospholipid levels of LA, ALA and long-chain polyunsaturated fatty acids during pregnancy, lactation, and may influence an infant's IQ, atopy and coronary heart disease (CHD) risk. At low intakes of eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), polymorphisms at the 5-lipoxygenase (5-LO) level increase the risk for CHD whereas polymorphisms at cyclooxgenase-2 increase the risk for prostate cancer. At high intakes of LA the risk for breast cancer increases. EPA and DHA influence gene expression. In future, intervention studies on the biological effects of LA, ALA and LC-PUFAs, and the effects of genetic variants in FADS1 and FADS2, 5-LO and cyclooxygenase-2 should be taken into consideration both in the determination of nutritional requirements and chronic disease risk. Furthermore, genome-wide association studies need to include environmental exposures and include diet in the interaction between genetic variation and disease association.

[pibikay]

Interesting. What does FADS stand for?

[Jackie07]

Am J Clin Nutr. 2010 May;91(5):1368-76. Epub 2010 Mar 24.
FADS1 FADS2 gene variants modify the association between fish intake and the docosahexaenoic acid proportions in human milk.

Moltó-PuigmartÃ* C, Plat J, Mensink RP, Müller A, Jansen E, Zeegers MP, Thijs C.
Department of Nutrition and Food Science, Faculty of Pharmacy, University of Barcelona, Barcelona, Spain.
Abstract

BACKGROUND: The genes encoding Delta(5)- and Delta(6)-desaturases (FADS1 FADS2 gene cluster) were reported to be associated with n-3 (omega-3) and n-6 (omega-6) fatty acid proportions in human plasma, tissues, and milk. Docosahexaenoic acid (DHA) can be supplied especially by dietary fish or fish oil and synthesized from alpha-linolenic acid through a pathway involving these desaturases.
OBJECTIVE: We evaluated whether FADS gene variants modify the effect of maternal fish and fish-oil intake on plasma and milk DHA proportions.
DESIGN: FADS1 rs174561, FADS2 rs174575, and intergenic rs3834458 single nucleotide polymorphisms were genotyped in 309 women from the KOALA Birth Cohort Study in The Netherlands. Plasma was collected at 36 wk of pregnancy, and milk was collected at 1 mo postpartum. Fish and fish-oil intake was assessed by using a food-frequency questionnaire at 34 wk of pregnancy and updated for the week of milk collection. Gene-diet interactions were tested by linear regression analysis.
RESULTS: DHA proportions were lower in women homozygous for the minor allele than in women who were homozygous for the major allele (DHA proportions in plasma phospholipids: P < 0.01; DHA proportions in milk: P < 0.05). Fish intake ranged from 0 to 2.5 portions of fatty fish/wk, and 12 women took fish-oil supplements during pregnancy. DHA proportions in plasma phospholipids increased with increasing fish and fish-oil intake, irrespective of the genotype. DHA proportions in milk increased only with fish and fish-oil intake in the major-allele carriers.
CONCLUSION: Lower proportions of DHA in milk from women who were homozygous for the minor allele could not be compensated for by increasing fish and fish-oil intake, possibly because of limited incorporation into milk.

[R.B.]

pibikay

^ This may help

FADS = Fatty acid desaturase

http://en.wikipedia.org/wiki/Fatty_acid_desaturase


Jackie 07

Could the failure of dietary DHA to raise DHA in breast milk be because even with additional intake the women were still not making enough to meet the needs of the foetus / their own needs and that higher intakes than used may have raised levels in breast milk. Other papers seem to suggest that in general supplementation raises DHA in breast milk

The effects of fish oil supplementation in pregnancy on breast milk fatty acid composition over the course of lactation: a randomized controlled trial.

Dunstan JA, Mitoulas LR, Dixon G, Doherty DA, Hartmann PE, Simmer K, Prescott SL.

School of Paediatrics and Child Health, The University of Western Australia, Crawley WA 6009.
Abstract

This study evaluated the longitudinal effect of fish oil in pregnancy on breast milk fatty acid composition and infant outcomes. In a randomized, controlled trial, 98 women received 2.2 g docosahexaenoic acid (DHA) and 1.1 g eicosapentaenoic acid (EPA) or olive oil from 20 wk of gestation until delivery. Fatty acid composition in breast milk (at 3 d, 6 wk, and 6 mo) and infant erythrocyte membranes (at 1 y) were determined by gas liquid chromatography. Breast milk fatty acids were examined in relationship to growth and development. Compared with control group, breast milk from women who received fish oil had proportionally higher DHA and EPA levels at 3 d and 6 wk after delivery, but this difference was no longer apparent by 6 mo. Infant DHA status at 1 y of age was directly related to DHA levels at 3 d, 6 wk, and 6 mo postpartum (but not to antenatal supplementation). Both EPA and DHA in breast milk were positively correlated with Griffith's developmental scores including hand and eye coordination. Thus, supplementation in pregnancy was associated with increased n-3 long-chain polyunsaturated fatty acids (LCPUFAs) in breast milk, particularly in early lactation, and this was positively associated with infant DHA status at 1 y.

Thanks for posting that link I will bear the contents in mind.

[R.B.]

More emphasis as to the importance of fats in cancer.


Cancer Biol Ther. 2011 Apr 15;11(8):724-31. Epub 2011 Apr 15.
Fatty acids as potential adjunctive colorectal chemotherapeutic agents.
Fauser JK, Prisciandaro LD, Cummins AG, Howarth GS.
Source

University of Adelaide, Adelaide, Australia; The Queen Elizabeth Hospital, Woodville, South Australia, Australia.
Abstract

Fatty acids (FA) are bioactive molecules which have potential as adjunctive chemotherapeutic agents. FA are classified as short-, medium; or long-chain on the basis of the number of carbon atoms in the aliphatic chain and have been reported to induce apoptosis in vitro in a range of cancer cell types, including breast, tongue, cervix and colorectal. However, to date the chain length exerting optimal anti-neoplastic properties remains undefined. Short chain fatty acids, such as butyrate (C4:0), have induced high rates of in vitro apoptosis, presumably related to epigenetic modification, cell cycle arrest and activation of pro-apoptotic genes. Medium chain fatty acids have demonstrated in vivo and in vitro cytotoxic and anti-microbial properties; however, scant evidence currently exists on their anti-neoplastic potential. Longer unsaturated fatty acids (C16-24: ω3-9), including conjugated linoleic acid and eicosapentaenoic acid, also exhibit in vitro anti-proliferative actions, including induction of oxidative stress and modification of intracellular signalling pathways. Although incorporation of FA into CRC chemotherapy regimens is in its infancy, evidence is accumulating to allow identification of the FA chain length capable of exerting the most effective anti-neoplastic activity.

PMID:
21430438
[PubMed - in process]

[R.B.]

In essence the fat composition of the breast tissue is diet sensitive.

A trial looking at the impact of dietary EPA + DHA suggests that in terms of tissue composition there was not any significant benefit in more that 2.52 grams a day.


Full Free Text



http://www.ncbi.nlm.nih.gov/pmc/arti...tool=pmcentrez

ω-3 Fatty acid supplements in women at high risk of breast cancer have dose-dependent effects on breast adipose tissue fatty acid composition1,2,3
Lisa D Yee,corresponding author Joanne L Lester, Rachel M Cole, Julia R Richardson, Jason C Hsu, Yan Li, Amy Lehman, Martha A Belury, and Steven K Clinton

Background: Preclinical evidence of the preventive benefits of ω-3 (n–3) polyunsaturated fatty acids (PUFAs) in breast cancer continues to fuel interest in the potential role of dietary fat content in reducing breast cancer risk. The dose of fish-oil/ω-3 PUFAs needed to achieve maximal target tissue effects for breast cancer prevention remains undefined.
Objective: To determine the dose effects of ω-3 fatty acids on breast adipose tissue fatty acid profiles, we conducted a study of 4 doses of ω-3 PUFAs in women at high risk of breast cancer.
Design: In this 6-mo randomized open-label study, 48 women with increased breast cancer risk received 1, 3, 6, or 9 capsules/d of an ω-3 PUFA supplement that provided 0.84, 2.52, 5.04, and 7.56 g docosahexaenoic acid (DHA) + eicosapentaenoic acid (EPA) daily, respectively. Subjects made monthly visits, at which time pill counts were made and fasting blood samples were collected to determine fatty acid profiles; anthropometric measurements were made, breast adipose tissue samples were collected, and laboratory tests of toxicity (alanine aminotransferase, LDL cholesterol, and platelet function) were made at baseline and at 3 and 6 mo.
Results: All doses led to increased serum and breast adipose tissue EPA and DHA concentrations, but the response to 0.84 g DHA+EPA/d was less than the maximum possible response with ≥2.52 g/d. Body mass index attenuated the dose response for serum tissue DHA and EPA (P = 0.015 and 0.027, respectively) and breast adipose tissue DHA (P = 0.0022) in all of the treatment groups. The incremental increase in DHA and EPA correlated inversely with baseline fat and serum values. Compliance over 6 mo was 92.9 ± 9.2% and was unaffected by treatment arm. No severe or serious toxicities were reported.

Conclusions: Daily doses up to 7.56 g DHA+EPA were well tolerated with excellent compliance in this cohort at high risk of breast cancer. Body mass index and baseline fatty acid concentrations modulated the dose-response effects of ω-3 PUFA supplements on serum EPA and DHA and breast adipose tissue DHA.

[pibikay]

Thanks All.We have been away for a week at Kangra Valley in Himachal.Hence my late reply

[R.B.]

http://www.ncbi.nlm.nih.gov/pubmed/21569413

Lipids Health Dis. 2011 May 12;10(1):73. [Epub ahead of print]
Effects of n-3 PUFAs on breast cancer cells through their incorporation in plasma membrane.
Corsetto PA, Montorfano G, Zava S, Jovenitti IE, Cremona A, Berra B, Rizzo AM.
Abstract

ABSTRACT:
BACKGROUND:

PUFAs are important molecules for membrane order and function; they can modify inflammation-inducible cytokines production, eicosanoid production, plasma triacylglycerol synthesis and gene expression. Recent studies suggest that n-3 PUFAs can be cancer chemopreventive, chemosuppressive and auxiliary agents for cancer therapy. PUFAs could alter cancer growth influencing cell replication, cell cycle, and cell death. The question that remains to be answered is how n-3 PUFAs can affect so many physiological processes. We hypothesize that n-3 PUFAs alter membrane stability, modifying cellular signalling in breast cancer cells.
METHODS:

Two lines of human breast cancer cells characterized by different expression of ER and EGFR receptors were treated with AA, EPA or DHA. We have used the MTT viability test and expression of apoptotic markers to evaluate the effect of PUFAs on cancer growth. Phospholipids were analysed by HPLC/GC, to assess n-3 incorporation into the cell membrane.
RESULTS:

We have observed that EPA and DHA induce cell apoptosis, a reduction of cell viability and a decrease of Bcl2 and procaspase-8 expression. Moreover, DHA slightly reduces the concentration of EGFR but EPA has no effect. Both EPA and DHA reduce the activation of EGFR. N-3 fatty acids are partially metabolized in both cell lines; AA is integrated without being further metabolized. We have analysed the fatty acid pattern in membrane phospholipids where they are incorporated with different degrees of specificity. N-3 PUFAs influence the n-6 content and vice versa.
CONCLUSIONS:

Our results indicate that n-3 PUFA feeding might induce modifications of breast cancer membrane structure that increases the degree of fatty acid unsaturation. This paper underlines the importance of nutritional factors on health maintenance and on disease prevention.

[R.B.]

Effects of n-3 PUFAs on breast cancer cells through their incorporation in plasma membrane
Paola A Corsetto,1 Gigliola Montorfano,1 Stefania Zava,1 Ilaria E Jovenitti,1 Andrea Cremona,1 Bruno Berra,1 and Angela M Rizzocorresponding author1
1Dipartimento di Scienze Molecolari Applicate ai Biosistemi, UniversitÃ* degli Studi di Milano, Italy

(Full Free Text)

http://www.ncbi.nlm.nih.gov/pmc/arti...tool=pmcentrez

Background
PUFAs are important molecules for membrane order and function; they can modify inflammation-inducible cytokines production, eicosanoid production, plasma triacylglycerol synthesis and gene expression. Recent studies suggest that n-3 PUFAs can be cancer chemopreventive, chemosuppressive and auxiliary agents for cancer therapy. N-3 PUFAs could alter cancer growth influencing cell replication, cell cycle, and cell death. The question that remains to be answered is how n-3 PUFAs can affect so many physiological processes. We hypothesize that n-3 PUFAs alter membrane stability, modifying cellular signalling in breast cancer cells.

Methods
Two lines of human breast cancer cells characterized by different expression of ER and EGFR receptors were treated with AA, EPA or DHA. We have used the MTT viability test and expression of apoptotic markers to evaluate the effect of PUFAs on cancer growth. Phospholipids were analysed by HPLC/GC, to assess n-3 incorporation into the cell membrane.
Results
We have observed that EPA and DHA induce cell apoptosis, a reduction of cell viability and the expression of Bcl2 and procaspase-8. Moreover, DHA slightly reduces the concentration of EGFR but EPA has no effect. Both EPA and DHA reduce the activation of EGFR.
N-3 fatty acids are partially metabolized in both cell lines; AA is integrated without being further metabolized. We have analysed the fatty acid pattern in membrane phospholipids where they are incorporated with different degrees of specificity. N-3 PUFAs influence the n-6 content and vice versa.

Conclusions
Our results indicate that n-3 PUFA feeding might induce modifications of breast cancer membrane structure that increases the degree of fatty acid unsaturation. This paper underlines the importance of nutritional factors on health maintenance and on disease prevention.

[R.B.]

Hi All

Apologies I managed to duplicate a reference above.

The ongoing saga of dental infection continues, and my suspicion that dental infections can fog the brain remains. My childhood hockey accident broken root filled and refilled and apisectomied tooth [twice] appears to have been reinfecting the bone through escape of bacteria living in the space where the post sits - the tooth and a neighbouring tooth have now been removed - not a good look (-: - but hopefully the recurring infection in the bone in the area and likely higher in the face which has been going on to greater and lesser extent for several years, now may clear up.

This is a fascinating summary adding to the evidence excess linoleic acid (plant based 18 carbon Omega Six which makes up 50 - 70 % of the fat in many vegetable oils, and arguably which many of us get too much of) is a factor in BC.


Int J Biochem Cell Biol. 2011 Sep 16. [Epub ahead of print]
Linoleic acid induces an EMT-like process in mammary epithelial cells MCF10A.
Espinosa-Neira R, Mejia-Rangel J, Cortes-Reynosa P, Salazar EP.
Source

Departamento de Biologia Celular, Cinvestav-IPN, Av. IPN # 2508, San Pedro Zacatenco, Mexico, DF 07360, Mexico.
Abstract

Epidemiological studies and animal models suggest an association between high levels of dietary fat intake and an increased risk of developing breast cancer. Epithelial-mesenchymal-transition (EMT) is a process, by which epithelial cells are transdifferentiated to a mesenchymal state, and it has been implicated in cancer progression, including invasion and metastasis. Linoleic acid (LA) induces proliferation and invasion in breast cancer cells. However, the role of LA on the EMT process in human mammary epithelial cells remains to be studied. In the present study, we demonstrate that LA induces a transient down-regulation of E-cadherin expression, accompanied with an increase of Snail1, Snail2, Twist1, Twist2 and Sip1 expressions. Furthermore, LA induces FAK and NFκB activation, MMP-2 and -9 secretions, migration and invasion. In summary, our findings demonstrate, for the first time, that LA promotes an EMT-like process in MCF10A human mammary epithelial cells.

Copyright © 2011 Elsevier Ltd. All rights reserved.

PMID:
21945809
[PubMed - as supplied by publisher]

[R.B.]

More Omega 3 and 6 mechanisms which affect cancer cell function (-:

Omega 6 derivatives are the main natural activators of pathways in which cannabis derivatives are also active, which has a host of implications, including in controlling mood, food intake, weight gain etc. As well as influencing brain function these Omega 6 compounds are also active in many cells, including the reproductive system. This paper suggests they affect proliferation in cancer cells.

It looks as if Omega 3 derivatives have different roles in these pathways to Omega 6 derivatives and once again the balance between the two appears to affect cell function. ( FYI anandamide and 2-arachidonoylglycerol are omega 6 based products - see below)

The involvement of cannabis receptors begs the question does cannabis affect cancer (increase or decrease) by inhibiting the access of other compounds to these pathways - scientists are looking a the effects of cannabis derivatives on cancer - and that in turn would depend on the balance of natural activators produced in the body, including through the Omega 3 and 6 pathways but the wider implications ??? These receptors are found widely in the body including in the brain, and I value the function of mine.



Prostaglandins Leukot Essent Fatty Acids. 2011 Oct 11. [Epub ahead of print]
Omega-3 N-acylethanolamines are endogenously synthesised from omega-3 fatty acids in different human prostate and breast cancer cell lines.
Brown I, Wahle KW, Cascio MG, Smoum-Jaouni R, Mechoulam R, Pertwee RG, Heys SD.
Source

Translational Medical Sciences, Division of Applied Medicine, School of Medicine and Dentistry, University of Aberdeen, Aberdeen, AB25 2ZD, UK.
Abstract

Omega-3 (n-3) fatty acids inhibit breast and prostate cancer cell growth. We previously showed that N-acylethanolamine derivatives of n-3 (n-3-NAE) are endocannabinoids, which regulate cancer cell proliferation. These n-3-NAE are synthesised in certain cells/tissues, after supplementing with fatty acids, however, no one has assessed whether and to what extent this occurs in cancer cells. We determined levels of endogenous n-3-NAEs in hormone sensitive and insensitive prostate and breast cancer cells and subsequent effects on other endocannabinoids (anandamide and 2-arachidonoylglycerol), before and after supplementing with DHA and EPA fatty acids, using HPLC tandem mass spectrometry. This is the first study reporting that n-3-NAEs are synthesised from their parent n-3 fatty acids in cancer cells, regardless of tumour type, hormone status or the presence of fatty acid amide hydrolase. This could have important implications for the use of n-3 fatty acids as therapeutic agents in breast and prostate cancers expressing cannabinoid receptors.

Copyright © 2011 Elsevier Ltd. All rights reserved.

PMID:
21995886
[PubMed - as supplied by publisher]

[R.B.]

This is neat because it relates the Omega 3:6 profile of strictly controlled diet to what is happening in prostate cancer cells in living humans. The diet was tested in the time frame whilst patients were awaiting surgical removal of cancerous tissue, which tissue was then available for examination as to the effect of the different diets on cancer cell fat composition, structure, cell division rate, etc. The trial is small but has prompted a bigger trial


http://www.newswise.com/articles/you...e-cancer-cells

You are What You Eat: Low-Fat Diet with Fish Oil Slowed Growth of Human Prostate Cancer Cells
Released: 10/25/2011 7:00 AM EDT
Source: University of California, Los Angeles (UCLA), Health Sciences

"Newswise — A low-fat diet with fish oil supplements eaten for four to six weeks prior to prostate removal slowed down the growth of prostate cancer cells – the number of rapidly dividing cells – in human prostate cancer tissue compared to a traditional, high-fat Western diet.

Done by researchers at UCLA’s Jonsson Comprehensive Cancer Center, the short-term study also found that the men on the low-fat, fish oil supplement diet were able to change the composition of their cell membranes in both the healthy cells and the cancer cells in the prostate. They had increased levels of omega-3 fatty acids from fish oil and decreased levels of omega-6 fatty acids from corn oil in the cell membranes, which may directly affect the biology of the cells, though further studies are needed, said Dr. William Aronson, the study’s first author and a researcher with UCLA’s Jonsson Comprehensive Cancer Center.

The study also found that blood obtained from patients after the low-fat, fish oil diet program slowed the growth of prostate cancer cells in a test tube as compared to blood from men on the Western diet, which did not slow cancer growth.

“The finding that the low-fat, fish oil diet reduced the number of rapidly dividing cells in the prostate cancer tissue is important because the rate at which the cells are dividing can be predictive of future cancer progression,” Aronson said. “The lower the rate of proliferation, the lesser the chances that the cancer will spread outside the prostate, where it is much harder to treat.” . . .

"- the “treatment” was indeed reaching the targeted organ because of the changes in the prostate cell membrane’s fatty acid composition." . . .

"Diet studies often are difficult to evaluate because getting patients to comply with dietary changes can be challenging. However, the food eaten by men in both arms of this study was precisely controlled, Aronson said. The meals were prepared by chefs in the UCLA Clinical Translational Research Center and delivered in bulk to study participants several times a week. Participants also met with a dietician, kept food diaries and were required to return uneaten food."


"
The study appeared Oct. 25, 2011 in Cancer Prevention Research, a peer-reviewed journal of the American Association for Cancer Research."

[Andrea Barnett Budin]

For goodness sakes -- IS THERE NO END TO THE MANY WAYS IN WHICH OMEGA 3 BENEFITS US ALL...???

Hi, RB! Can you list some of the diseases and ailments Omega 3 can alter our lives? Just in a neat little package. (I've read your book, and am ever impressed with it's messages.)

I know people in their 40s, 50s, 60s, 70s, and 80s who are on to this life-saver!

I take 2 a day. Every day...

[R.B.]

The formation of blood vessels to supply a tumour, called 'angiogenisis', is a key part of cancer.

Some Omega 6 products increase of VGEF which promotes blood vessel formation.

This article recognises the role of Omega 3 but does not look in any depth at Omega 6.

Tumor Angiogenesis as a Target for Dietary Cancer Prevention

http://downloads.hindawi.com/journal...012/879623.pdf


HER2 is listed as a promoter of angiogenisis

This is a fascinating article on the topic which can be read free.

The article looks at how many of us carry cancerous cells and very small cancers saying

"Microscopic cancer cells are commonly present in the healthy adult, the result of errors during replication of 60–90 trillion cells."


It looks a evidence that many foods may play a part in controlling new blood vessel production.

Some suggest that those with hormone sensitive cancer should be careful about taking Resveratrol.

[R.B.]

More evidence that Omega 6 linoleic acid has a potential role in the development and spread of breast and logically other cancers.

An explanation for 'Epithelial-mesenchymal-transition' can be found at this wiki link
http://en.wikipedia.org/wiki/Epithel...mal_transition

Cadherins are proteins a bit like living velcro that help keep cells anchored to each other. Vitamin D reportedly increases adhesion between cells. In contrast this paper suggests Omega 6 linoleic acid weakens them, which would tie in with other reading


Int J Biochem Cell Biol. 2011 Dec;43(12):1782-91. Epub 2011 Sep 16.
Linoleic acid induces an EMT-like process in mammary epithelial cells MCF10A.
Espinosa-Neira R, Mejia-Rangel J, Cortes-Reynosa P, Salazar EP.
Source

Departamento de Biologia Celular, Cinvestav-IPN, Av. IPN # 2508, San Pedro Zacatenco, Mexico, DF 07360, Mexico.
Abstract

Epidemiological studies and animal models suggest an association between high levels of dietary fat intake and an increased risk of developing breast cancer. Epithelial-mesenchymal-transition (EMT) is a process, by which epithelial cells are transdifferentiated to a mesenchymal state, and it has been implicated in cancer progression, including invasion and metastasis. Linoleic acid (LA) induces proliferation and invasion in breast cancer cells. However, the role of LA on the EMT process in human mammary epithelial cells remains to be studied. In the present study, we demonstrate that LA induces a transient down-regulation of E-cadherin expression, accompanied with an increase of Snail1, Snail2, Twist1, Twist2 and Sip1 expressions. Furthermore, LA induces FAK and NFκB activation, MMP-2 and -9 secretions, migration and invasion. In summary, our findings demonstrate, for the first time, that LA promotes an EMT-like process in MCF10A human mammary epithelial cells.

[Ellie F]

Thanks RB for the interesting article from hindawi.
Ellie

[karen z]

o.k., RB,
I am feeling a bit tired and would like to go to the punch line on this important thread. Could you (or someone) give me the short and sweet version (from any source) of a classic mediterranean diet? Perhaps a yes/no list (recipes along with that list would be great) but mostly the punchline. Sorry to be lazy!!!

[karen z]

Can anyone help with my request?
THANKS.

[Mtngrl]

Karen--

I'll take a stab at it, though R.B. is the expert. He even wrote a book on it.

In an early post it says: "The diet of our ancestors was less dense in calories, being higher in fiber, rich in fruits, vegetables, lean meat, and fish. As a result, the diet was lower in total fat and saturated fat, but contained equal amounts of n-6 and n-3 essential fatty acids. Linoleic acid (LA) is the major n-6 fatty acid, and alpha-linolenic acid (ALA) is the major n-3 fatty acid. In the body, LA is metabolized to arachidonic acid (AA), and ALA is metabolized to eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA)."

Translation: Nowadays, our diet has a much higher ratio of Omega 6 to Omega 3 than the diet we evolved on, both because we directly eat a lot of vegetable oils that are high in Omega 6 and because the animal foods that we consume (meat, eggs, milk, butter) have the same imbalance, because the animals were fed a high Omega 6 diet (i.e. grains and soy.)

The practical application is this: Eat a predominately plant-based diet of whole, unprocessed foods: whole grains, lots and lots of vegetables, and fruit. Eat wild, cold-water fish a few times a week. If you can get it, eat "pastured" (grass fed) meat, eggs, butter and milk. Milk from grass fed cows is higher in Omega 3 fatty acids than conventional milk, and it has conjugated linoleic acid, which is good for you, and which conventional milk does not have. If you can't get red meat, chicken, eggs and dairy foods from grass fed animals, consider skipping them or severely limiting them. (Nonfat dairy foods should be alright--no fat means no imbalance of fats, I should think.) Don't eat anything fried. Use just a little olive oil on your salads. Avoid all trans fats (hydrogenated fats). Avoid or limit added sugar. Don't use artificial sweeteners.

You might want to take fish oil supplements--one or two grams a day. If you are a vegetarian, flax seed is high in Omega-3, but it is a kind that your body has to convert to be useful. Some people's bodies do this better than others'.

For breast cancer, the question of drinking red wine, which is another component of the "Mediterranean Diet," is controversial. At least one researcher thinks it's fine to have one glass a day with a meal of the "right" foods. The consensus, however, seems to be to the contrary.

One "flat belly" diet program based on the Mediterranean diet says to eat monounsaturated fatty acids with each meal. Sources include olives, dark chocolate, olive oil, avocado, cashew, sesame, and other nuts. But fats are very nutrient dense, and as the opening sentence stated, we evolved on a less dense, lower-fat diet than we typically eat now.