The traditional diet of Greece and cancer.

[Heart Sutra]

Diet has been pretty well established to be of such individual affect, that an all encompassing dietary solution working for all people is rather unlikely. Of course, eating pretzels and malt balls is probably less helpful than eating a more balanced diet...

R.B. just curious as to your diagnosis and history, I don't see one added to your profile.

Thank you for being here and for offering all of the information that you do.

Kevin and Sue

[R.B.]

Heart Sutra

I have previously openly declared I am a male with an interest in the impact of omega six and omega three on a range of conditions, functions of the body etc. I am strictly amateur but do read widely. I am learning too. I do try and practice what I suggest, but could do better.

I had a relative who died of BC. I had a lump excised which was not likely to be BC but could have been and the experience was thought provoking.



RE your comment - "that an all encompassing dietary solution working for all people is rather unlikely"

Our bodies all function at a basic level in very similar ways. The food you eat alters the way you express your genes - the number of copies you switch on including HER2 and BRAC.

Trials on other issues such as cardiac health have shown in general terms people respond similarly to a low fat low protein "healthy" diet, (following general recommendations above).

Our modern diet breaks so many of the basic rules that we are not talking about fine tuning - this is about the basics. We have evolved / been designed to live in an environment with a range of diets, but those never included refined foods, high levels of sugars, salt, trans fats, vegetable oils. These push the body outside its design parameters. The consequence is a greatly increased of range of conditions.

There is a strong argument that better diet for those who eat high levels of refined food...... will reduce the risk for all [some more than others and on the average]

Of course once you have the basics sorted out one could consider fine tuning but the problem is it is very difficult to know exactly what does what. Given we were used to a much wider variety than we have now and plants are a veritable natural pharmacy (a mixture of positive and negative both of which the body can use - to support, or utilise in its armoury) variety seems a good strategy.

The China Study (about $20 US new)

http://www.thechinastudy.com/about.html

It is a very though provoking read. I have questions as to whether his conclusions would have changed in any way if he had looked at the omega three six issues. He touches on fish as a protein source but there is not much on it either way in his book. (eg Eskimos would be a fish exception to the no protein rule) The fat that goes with meat protein is clearly an issue and strict moderation likely sensible as a minimum.

I would also highly recommend Smart Fats M Schmidt (there is a newer version) which is also very thought provoking.

RB

[R.B.]

Just bringing this back up for new readers and adding a cross link to try and keep key material in one thread.



http://www.her2support.org/vbulletin...ad.php?t=28215

RB

[R.B.]

A useful diet link to add to the thread (also posted in articles of interest but putting a copy here makes it easier to find for those starting out)


http://www.pubmedcentral.nih.gov/art...z&artid=526387


Nutrition and cancer: A review of the evidence for an anti-cancer diet
Michael S Donaldsoncorresponding author1
1Director of Research, Hallelujah Acres Foundation, 13553 Vantage Hwy, Ellensburg, WA 98926, USA

t has been estimated that 30–40 percent of all cancers can be prevented by lifestyle and dietary measures alone. Obesity, nutrient sparse foods such as concentrated sugars and refined flour products that contribute to impaired glucose metabolism (which leads to diabetes), low fiber intake, consumption of red meat, and imbalance of omega 3 and omega 6 fats all contribute to excess cancer risk. Intake of flax seed, especially its lignan fraction, and abundant portions of fruits and vegetables will lower cancer risk. Allium and cruciferous vegetables are especially beneficial, with broccoli sprouts being the densest source of sulforophane. Protective elements in a cancer prevention diet include selenium, folic acid, vitamin B-12, vitamin D, chlorophyll, and antioxidants such as the carotenoids (α-carotene, β-carotene, lycopene, lutein, cryptoxanthin). Ascorbic acid has limited benefits orally, but could be very beneficial intravenously. Supplementary use of oral digestive enzymes and probiotics also has merit as anticancer dietary measures. When a diet is compiled according to the guidelines here it is likely that there would be at least a 60–70 percent decrease in breast, colorectal, and prostate cancers, and even a 40–50 percent decrease in lung cancer, along with similar reductions in cancers at other sites. Such a diet would be conducive to preventing cancer and would favor recovery from cancer as well.

[R.B.]

Just to bump this up for any new visitors.

RB

[R.B.]

Just bumping back up for those that might not have seen the thread.

RB

[Lauriesh]

Bump


Laurie

[R.B.]

Just bringing it back up for new members in case of interest

[hutchibk]

Thanks for the bumps, as I had lost track of this thread and it is a very important one! I want to switch my entire diet (at least home cooked diet) to the healthiest aspects of Med/Greek. I have always loved the food, the freshness, the oils, etc...

[R.B.]

The first trial you have seen before I think the rest a new here.

Just in case you have lost sight of the omega threes and sixes

RB



http://www.ncbi.nlm.nih.gov/sites/en...ubmed_RVDocSum

"These findings reveal that the omega-3 PUFA ALA suppresses overexpression of HER2 oncogene at the transcriptional level, which, in turn, interacts synergistically with anti-HER2 trastuzumab- based immunotherapy. ii) Our results molecularly support a recent randomized double-blind placebo-controlled clinical trial suggesting that ALA may be a potential dietary alternative or adjunct to currently used drugs in the management of HER2-positive breast carcinomas. iii) Considering our previous findings demonstrating the HER2 upregulatory actions of the omega-6 PUFA linolenic acid (LA; 18:2n-6) and the HER2 down-regulatory actions of the omega-3 PUFA docosahexaenoic acid (DHA; 22:6n-3) and of the omega-9 monounsaturated fatty acid oleic acid (OA; 18:1n-9), it is reasonable to suggest that a low omega-6/omega-3 PUFA ratio and elevated MUFA levels, the two prominent fat features of the Mediterranean diet, should be extremely efficient at blocking HER2 expression in breast cancer cells."


http://www.ncbi.nlm.nih.gov/sites/en...ubmed_RVDocSum

"our results indicate that (n-3) FA modify the lipid composition of membrane rafts and alter EGFR signaling in a way that decreases the growth of breast tumors."

http://www.ncbi.nlm.nih.gov/sites/en...ubmed_RVDocSum

"Use of canola oil instead of corn oil in the diet may be a reasonable means to increase consumption of n-3 fatty acids with potential significance for slowing growth of residual cancer cells in cancer survivors."

http://www.ncbi.nlm.nih.gov/sites/en...ubmed_RVDocSum

"In conclusion, we showed that erythrocyte compositions of specific fatty acids derived from fish intake, as biomarkers, are associated with lower risk of breast cancer, but further studies are needed to investigate mechanisms linked to the etiology. (c) 2007 Wiley-Liss, Inc."

http://www.ncbi.nlm.nih.gov/sites/en...ubmed_RVDocSum

"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."

http://www.ncbi.nlm.nih.gov/sites/en...ubmed_RVDocSum

"Our results support the premise that DHA and genistein exert complementary actions whilst genistein is antagonistic to AA for controlling PGE(2) production as well as invasiveness of MDA-MB-231 cells in culture by modulating the level of NFkappaB expression."

[R.B.]

Just bumping this up and adding a few bits I came across by accident whilst looking for something else.

RB


CoQ10.

Very small numbers and not much detail but thought provoking.

Views on CoQ10 vary amongst oncologists so please discuss any supplementation with your advisor.

I simply seek to inform options.

RB


1: Clin Biochem. 2000 Jun;33(4):279-84.Click here to read Links
Coenzyme Q10 concentrations and antioxidant status in tissues of breast cancer patients.
Portakal O, Ozkaya O, Erden Inal M, Bozan B, Koşan M, Sayek I.

Department of Biochemistry, The Medical School of Osmangazi University, Eskişehir, Turkey. portakal@ada.net.tr

OBJECTIVES: An increasing amount of experimental and epidemiological evidence implicates the involvement of oxygen derived radicals in the pathogenesis of cancer development. Oxygen derived radicals are able to cause damage to membranes, mitochondria, and macromolecules including proteins, lipids and DNA. Accumulation of DNA damages has been suggested to contribute to carcinogenesis. It would, therefore, be advantageous to pinpoint the effects of oxygen derived radicals in cancer development. DESIGN AND METHODS: In the present study, we investigated the relationship between oxidative stress and breast cancer development in tissue level. Breast cancer is the most common malignant disease in Western women. Twenty-one breast cancer patients, who underwent radical mastectomy and diagnosed with infiltrative ductal carcinoma, were used in the study. We determined coenzyme Q10 (Q) concentrations, antioxidant enzyme activities (mitochondrial and total superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), catalase), and malondialdehyde (MDA) levels in tumor and surrounding tumor-free tissues. RESULTS: Q concentrations in tumor tissues significantly decreased as compared to the surrounding normal tissues (p < 0.001). Higher MDA levels were observed in tumor tissues than noncancerous tissues (p < 0.001). The activities of MnSOD, total SOD, GSH-Px and catalase in tumor tissues significantly increased (p < 0.001) compared to the controls. CONCLUSIONS: These findings may support that reactive oxygen species increased in malignant cells, and may cause overexpression of antioxidant enzymes and the consumption of coenzyme Q10. Increased antioxidant enzyme activities may be related with the susceptibility of cells to carcinogenic agents and the response of tumor cells to the chemotherapeutic agents. Administration of coenzyme Q10 by nutrition may induce the protective effect of coenzyme Q10 on breast tissue.

PMID: 10936586 [PubMed - indexed for MEDLINE]

http://www.ncbi.nlm.nih.gov/sites/en...ubmed_RVDocSum


Progress on therapy of breast cancer with vitamin Q10 and the regression of metastases.
Lockwood K, Moesgaard S, Yamamoto T, Folkers K.

Pharma Nord, Vejle, Denmark.

Over 35 years, data and knowledge have internationally evolved from biochemical, biomedical and clinical research on vitamin Q10 (coenzyme Q10; CoQ10) and cancer, which led in 1993 to overt complete regression of the tumors in two cases of breast cancer. Continuing this research, three additional breast cancer patients also underwent a conventional protocol of therapy which included a daily oral dosage of 390 mg of vitamin Q10 (Bio-Quinone of Pharma Nord) during the complete trials over 3-5 years. The numerous metastases in the liver of a 44-year-old patient "disappeared," and no signs of metastases were found elsewhere. A 49-year-old patient, on a dosage of 390 mg of vitamin Q10, revealed no signs of tumor in the pleural cavity after six months, and her condition was excellent. A 75-year-old patient with carcinoma in one breast, after lumpectomy and 390 mg of CoQ10, showed no cancer in the tumor bed or metastases. Control blood levels of CoQ10 of 0.83-0.97 and of 0.62 micrograms/ml increased to 3.34-3.64 and to 3.77 micrograms/ml, respectively, on therapy with CoQ10 for patients A-MRH and EEL.

PMID: 7612003 [PubMed - indexed for MEDLINE]


http://www.ncbi.nlm.nih.gov/sites/en...ubmed_RVDocSum




1: Biochem Biophys Res Commun. 1994 Mar 30;199(3):1504-8.Click here to read Links
Partial and complete regression of breast cancer in patients in relation to dosage of coenzyme Q10.
Lockwood K, Moesgaard S, Folkers K.

Pharma Nord, Vejle, Denmark.

Relationships of nutrition and vitamins to the genesis and prevention of cancer are increasingly evident. In a clinical protocol, 32 patients having -"high-risk"- breast cancer were treated with antioxidants, fatty acids, and 90 mg. of CoQ10. Six of the 32 patients showed partial tumor regression. In one of these 6 cases, the dosage of CoQ10 was increased to 390 mg. In one month, the tumor was no longer palpable and in another month, mammography confirmed the absence of tumor. Encouraged, another case having a verified breast tumor, after non-radical surgery and with verified residual tumor in the tumor bed was then treated with 300 mg. CoQ10. After 3 months, the patient was in excellent clinical condition and there was no residual tumor tissue. The bioenergetic activity of CoQ10, expressed as hematological or immunological activity, may be the dominant but not the sole molecular mechanism causing the regression of breast cancer.

PMID: 7908519 [PubMed - indexed for MEDLINE]


http://www.ncbi.nlm.nih.gov/sites/en...ubmed_RVDocSum


1: Biochem Biophys Res Commun. 1997 May 19;234(2):296-9.Click here to read Links
Activities of vitamin Q10 in animal models and a serious deficiency in patients with cancer.
Folkers K, Osterborg A, Nylander M, Morita M, Mellstedt H.

Institute for Biomedical Research, University of Texas at Austin, 78712, USA.

New data on blood levels of vitamin Q10 in 116 cancer patients reveal an incidence of 23.1% of patients (N=17) with breast cancer whose blood levels were below 0.5 microg/ml. The incidence of breast cancer cases with levels below 0.6 microg/ml was 38.5%. The incidence is higher (p<0.05) than that for a group of ordinary people. Patients (N=15) with myeloma showed a mean blood level of 0.67 +/- 0.17 microg/ml. The incidence of a vitamin Q10 blood level below 0.7 microg/ml for these 15 cases of myeloma was 53.3%, which is higher (p<0.05) than the 24.5% found for a group of ordinary people.

PMID: 9177262 [PubMed - indexed for MEDLINE]

[R.B.]

Just bumping this thread up again.

This is a link I found recently which is by the renowned expert AP Simopoulos.

Only the first section is free. It is well worth reading. It really emphasises the need to balance the omega three and sixes.

http://content.karger.com/ProdukteDB...searchParm=toc

It is great to see this thread is slowly building up a significant number of hits. It would be interesting to know now many come from outside the board so hopefully bringing in new visitors.

Thank you for your interest.

R.B.

[R.B.]

Balancing the omega 3s and 6s - why - an experts explanation.

William Lands in a hero in the lipids world and continues to press his cause.

Eicosanoids are chemicals made from the omega three and sixes families that are huegely influential in the body. The chemicals are unique to each fat. It is a complex subject but you do not need to know the detail to get the gist that balancing the omega threes and sixes is a good risk reduction policy as part of a dietary strategy.

As always please discuss dietary change with your doctor.

The video below is worth looking at if you have the time. (about 18 mins)

One senses from the video that William Lands is an inspirational character.

RB

http://videocast.nih.gov/ram/crii01c303202000.ram


Monday, March 20, 2000
Author/Sponsor: Bill Lands, Ph.D., Senior Advisor, NIAAA, NIH
Total Running Time: 00:18:45
Bandwidth: 146 Kbps
This is a work of the United States Government. No copyright exists on this material.

[R.B.]

If you enjoyed that last video lecture you may enjoy this.

I only found it recently. It is fascinating for those who are interested.

Thank you Professor White for an excellent and fascinating lecture.

http://videocast.nih.gov/ram/crii01c303202000.ram

It is more technical but it does emphasise the power and importance of omega three and particularly the products of omega six. You don't need to understand it all just to understand how important they are in the body. Don't worry to much about the terminology they are just all omega six chemical products.

It is understandable.
n3 = omega three
n6 = omega six
Eicosanoids = omega three or six chemicals.
Arachidonic acid = child of omega six (long chain omega six equivalent to EPA)

It also gives an inkling as to how wondrous it all is and why it is necessary to give the body the raw material it needs as substitutes wont work the same way.

Note the slide at the end where for the pathway under consideration DHA is a more effective cox blocker than many drugs.

Other pathways in the same family connect into blood vessel growth and oestrogen levels, and hence the relevance to BC, and why it is now beginning to be suggested that Cox blockers may reduce the BC risk.

It is complicated.

So the message is as ever to reduce the risk profile of a number of conditions including BC balance your omega threes and sixes within reasonable limits and ensure a supply of long chain omega threes.

Please discuss dietary change with your medical advisor.


RB

[R.B.]

Benefits of omega threes again.

This also looks at saturated fats and it appears some saturated fats are associated with a lower risk of BC but I have not seen the full report as it is pay for view.

RB

Apr 2007
Erythrocyte fatty acids and breast cancer risk: a case-control study in Shanghai, China.
Shannon J, King IB, Moshofsky R, Lampe JW, Gao DL, Ray RM, Thomas DB.

Center for Research on Occupational and Environmental Toxicology, Oregon Health and Science University, Portland, OR,

Abstract

"CONCLUSION: Our results support a protective effect of n-3 fatty acids on breast cancer risk and provide additional evidence for the importance of evaluating the ratio of fatty acids when evaluating diet and breast cancer risk."

http://www.ncbi.nlm.nih.gov/sites/en...RVAbstractPlus

[R.B.]

This emphasises the difference between oils with differing omega three content.

Unfortunately no information is given on the omega six content of the oils used.

RB



Dietary canola oil suppressed growth of implanted MDA-MB 231 human breast tumors in nude mice.
Hardman WE.

The Department of Biochemistry and Microbiology, Marshall University School of Medicine, Huntington, West Virginia 25701, USA. hardmanw@marshall.edu

Abstract

"Use of canola oil instead of corn oil in the diet may be a reasonable means to increase consumption of n-3 fatty acids with potential significance for slowing growth of residual cancer cells in cancer survivors."

http://www.ncbi.nlm.nih.gov/sites/en...ubmed_RVDocSum

[R.B.]

EPA and DHA act as Cox 2 blockers.

Genistein acts as a Cox blocker.

Genistein acts synergistically with DHA.

AA the daughter omega six increased invasiveness as one would expect.

Genistein with omega threes uprates PPAR gamma which feature is in BC but I cannot remember how - or what relation this bears to omega six. So a ?? for the moment.

Genistein is an active ingredient in soy. There is much discussion if soy is good or bad.

So on balance more ticks for omega threes, crosses for omega six and a maybe for genestein via soy.

RB




Complementary actions of docosahexaenoic acid and genistein on COX-2, PGE2 and invasiveness in MDA-MB-231 breast cancer cells.
Horia E, Watkins BA.

Center for Enhancing Foods to Protect Health, Lipid Chemistry and Molecular Biology Laboratory, Purdue University, West Lafayette, IN 47907, USA.


Abstract

"The n-3 PUFA and genistein alone lowered PGE(2) concentration, and genistein in combination with AA reversed the high level of this prostanoid in cell cultures enriched with AA. The degree of cell invasiveness was reversed by genistein in cell cultures treated with AA and further reduced in those given DHA. The n-3 PUFA, in contrast to AA, reduced COX-2 and NFkappaB expression. Genistein combined with AA reversed the effects of AA alone on the expression of COX-2 and NFkappaB. All three fatty acids increased the expression of PPARgamma in the cells only when combined with genistein. Our results support the premise that DHA and genistein exert complementary actions whilst genistein is antagonistic to AA for controlling PGE(2) production as well as invasiveness of MDA-MB-231 cells in culture by modulating the level of NFkappaB expression."

[R.B.]

AndiBB pointed me to this trial. Thanks

Omega threes from whole fish are more effectively incorporated than fish oil.

Whole food sources have to be the best starting point.

This has to be balanced with the pollution issues dealt with in earlier parts of this thread.

And the good news is the fish oil is taken up.

I wonder if it varies with how and with what the fish oil is taken?

http://www.ncbi.nlm.nih.gov/sites/en...ubmed_RVDocSum

1: Lipids. 2006 Dec;41(12):1109-14.Links
Enhanced incorporation of n-3 fatty acids from fish compared with fish oils.
Elvevoll EO, Barstad H, Breimo ES, Brox J, Eilertsen KE, Lund T, Olsen JO, Osterud B.

Norwegian College of Fishery Science, Department of Marine Biotechnology, University of Tromsø, Norway. edel.elvevoll@nfh.uit.no


"In conclusion, fish consumption is more effective in increasing serum EPA and DHA than supplementing the diet with fish oil."

[R.B.]

Lipid raft is a description of a gang of fats that work as a unit in the cell membrane.

More potential benefts for omega three 3 and that omega six in large quantities has a negative impact.

RB




http://www.ncbi.nlm.nih.gov/sites/en...ubmed_RVDocSum

1: J Nutr. 2007 Mar;137(3):548-53.Click here to read Links

Comment in:
J Nutr. 2007 Mar;137(3):545-7.

(n-3) PUFA alter raft lipid composition and decrease epidermal growth factor receptor levels in lipid rafts of human breast cancer cells.
Schley PD, Brindley DN, Field CJ.

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

To determine the mechanism by which the (n-3) fatty acids (FA) eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) decrease proliferation and induce apoptosis in MDA-MB-231 human breast cancer cells, we examined the effects of EPA and DHA on the lipid composition of lipid rafts as well as epidermal growth factor receptor (EGFR) raft localization and phosphorylation. (n-3) FA (a combination of EPA and DHA) inhibited (P < 0.05) the growth of MDA-MB-231 cells by 48-62% in the presence and absence, respectively, of linoleic acid (LA). More EPA and DHA were incorporated into lipid rafts isolated from MDA-MB-231 cells after treatment with (n-3) FA compared with cells treated with LA (P < 0.05). EPA and DHA treatment decreased (P < 0.05) lipid raft sphingomyelin, cholesterol, and diacylglycerol content and, in the absence of LA, EPA and DHA increased (P < 0.05) raft ceramide levels. Furthermore, there was a marked decrease in EGFR levels in lipid rafts, accompanied by increases in the phosphorylation of both EGFR and p38 mitogen-activated protein kinase (MAPK), in EPA+DHA-treated cells (P < 0.05). As sustained activation of the EGFR and p38 MAPK has been associated with apoptosis in human breast cancer cells, our results indicate that (n-3) FA modify the lipid composition of membrane rafts and alter EGFR signaling in a way that decreases the growth of breast tumors.

PMID: 17311938 [PubMed - indexed for MEDLINE]

[R.B.]

Another one for the omega three collection

: Nutr Cancer. 1995;24(2):151-60.Links
Fatty acid composition of breast adipose tissue in breast cancer patients and in patients with benign breast disease.
Zhu ZR, Agren J, Männistö S, Pietinen P, Eskelinen M, Syrjänen K, Uusitupa M.

Department of Clinical Nutrition, University of Kuopio, Finland.

Fatty acid composition of triglycerides (TGs) and phospholipids (PLs) in breast adipose tissue was analyzed in 73 female breast cancer patients and 55 patients with benign breast disease. No differences were observed in the dietary intake of the major fatty acids (i.e., palmitic, stearic, oleic, and linoleic acids) or in the proportion of TGs and PLs in breast adipose tissue between the two groups. In postmenopausal women, however, the dietary intake of eicosapentaenoic acid (20:5n-3) and docosahexaenoic acid (22:6n-3) was significantly lower in the breast cancer patients than in patients with benign breast disease. Accordingly, the percentage of docosahexaenoic acid of PLs in breast adipose tissue was significantly lower in breast cancer patients than in patients with benign breast disease among postmenopausal women. The stage of the breast cancer did not contribute to the observed alterations of fatty acid composition of PLs. Consonant with the previous epidemiologic data, the present results suggest that intake of the long-chain n-3 fatty acids (mainly derived from fish) may have a protective effect against breast cancer, particularly in postmenopausal women.

PMID: 8584451 [PubMed - indexed for MEDLINE]