The traditional diet of Greece and cancer.

[R.B.]

More evidence that Omega 3s - and Omega 6s (in excess - ) have a role in breast cancer risk reduction.

(Ooops just noted that Lani is quicker off the mark than me - thanks Lani - http://her2support.org/vbulletin/showthread.php?t=59076 )

FAT1 is a mouse with a gene from a worm inserted that allows them to convert Omega 6 to Omega 3; normally mammals including humans cannot convert Omega 6 to Omega 3, and we must get it from our diet, which is why getting Omega 3 in the diet is so important. Fat1 mice tend to change enough Omega 6 into Omega 3 to create an equal balance of the two in their body.

They compared how implanted HER2 cells grew in FAT1 and normal wild type (WT) mice.

Both mice were fed the same diet which contained lots of Omega 6 and very little Omega 3 (Safflower oil), but FAT1 mice (-: unlike the WT mice )-: could make their own Omega 3.

The implanted HER2 tumors initially grew in both normal (WT) and FAT1 mice, and continued to grow in the normal WT mice -, but in contrast shrunk and eventually disappeared - in the FAT1 mice.

The tumors in the FAT1 mice contained much more EPA and DHA and a much better Omega 3:6 ratio -.


Clearly we are not FAT1 mice, but nonetheless the results are intriguing.


(15-HEPE, 17-HDHA and PGE3 are downstream Omega 3 products produced in the body
https://www.caymanchem.com/app/templ.../catalog/14990

WT is the normal mouse (Wild Type)




http://www.ncbi.nlm.nih.gov/pubmed/24052576

J Lipid Res. 2013 Sep 19. [Epub ahead of print]
Inhibition of the HER2 pathway by n-3 polyunsaturated fatty acids prevents breast cancer in fat-1 transgenic mice.
Zou Z, Bellenger S, Massey KA, Nicolaou A, Geissler A, Bidu C, Bonnotte B, Pierre AS, Minville-Walz M, Rialland M, Seubert J, Kang JX, Lagrost L, Narce M, Bellenger J.
Source

Universite de Bourgogne, France;
Abstract

Overexpression of the tyrosine kinase receptor ErbB2/HER2/Neu, occurs in 25% to 30% of invasive breast cancer (BC) with poor patient prognosis. Due to confounding factors, inconsistencies still remain regarding protective effects of n-3 polyunsaturated fatty acids (PUFA) on BC. We therefore evaluated whether fat-1 transgenic mice, endogenously synthesizing n-3 PUFA from n-6 PUFA, were protected against BC development and we then aimed to study in vivo a mechanism potentially involved in such protection. E0771 BC cells were implanted into fat-1 and wild-type (WT) mice. After tumorigenesis examination, we analyzed the expression of proteins involved in HER2 signaling pathway and lipidomic analyses were performed in tumor tissues and plasma. Our results showed that tumors totally disappeared by day 15 in fat-1 mice when they continued to grow up in the WT. This prevention can be related in part to significant repression of the HER2/beta-catenin signaling pathway and formation of significant levels of n-3 PUFAs derived bioactive mediators (particularly 15-HEPE, 17-HDHA and PGE3) in the tumor of fat-1 mice compared to WT. All together these data demonstrate an anti-BC effect of n-3 PUFAs through, at least in part, HER2 signaling pathway downregulation, and highlight the importance of gene-diet interactions in BC.

The full paper can be read free here (-: http://www.jlr.org/content/early/201...r.M042754.long and includes the comment below

"To test the hypothesis that balanced ratio of n-6/n-3 fatty acid is able to decrease the risk of
BC, we implanted E0771 mouse BC cells into the fat-1 and WT mice and examined the
tumorigenicity of inoculated tumor cells. As shown in Fig.1, there was a dramatic difference
in the tumor volume between fat-1 transgenic (n=10) and WT mice (n=6). Over an
observation period of 25 days, all mice initially developed a palpable tumor by day 7 but,
importantly, all the tumors in fat-1 mice never grew up more and all palpable tumors
disappeared at day 18. By contrast, all the tumors in wild-type mice continued to grow up
until host sacrifice. These findings clearly show that expression of fat-1 inhibits the growth of
BC cells in vivo and results in mammary tumor regression.
Inhibition"

"Tumor n-3 fatty acid enrichment and formation of PUFA-derived mediators
As shown in Fig. 3A, fatty acid composition of tumor total lipids revealed higher levels of
10
EPA (20:5n-3) and docosapentaenoic acid (DPA, 22:5n-3) in fat-1 transgenic mice compared
with WT animals, whereas AA (20:4n-6) was decreased by 70%. Interestingly, the n-6/n-3
PUFA ratio (Figure 3B) was significantly reduced in tumors from fat-1 mice (8.92±2.63)
compared to WT animals (30.51±6.99) despite the animals were fed the same diet. These
results indicate expression of fat-1 enriches the transgenic animals in n-3 PUFA at the
expense of n-6, giving a lower n-6/n-3 ratio."



The pictures of the dead mice and their tumors or lack of them are not pretty but exceptionally powerfully make the point of this important trial; and yes I do 'feel' for the mice. (page 27)

The graph of the relative tumor sizes is equally very powerful. (page 27)


All of which takes us back to a French paper in which it was noted that women with higher levels of DHA in breast tissue had a 70% lower risk of their excised breast tissue 'lumps' being cancerous

[R.B.]

This trial was mentioned in the paper above and is specifically relevant to HER2. I do not recall posting it before.

Essentially more of the same . . .

LA = linoleic acid the omega 6 found in quantity in most vegetable oils

Dietary fatty acids regulate the activation status of Her-2/neu (c-erbB-2) oncogene in breast cancer cells

http://annonc.oxfordjournals.org/con...5/11/1719.long

"This report shows, to the best of our knowledge for the first time, that dietary FAs previously characterized for either their breast cancer protective effect (ALA, EPA, DHA and OA) or its tumoricidal actions (GLA) significantly downregulate Her-2/neu ECD concentration and, consequently, the activation status of Her-2/neu in SK-Br3 and BT-474 human breast cancer cell lines, which contain Her-2/neu oncogene amplification. Remarkably, LA, a ω-6 FA with a strong tumorigenesis stimulating effect, significantly increased Her-2/neu ECD concentration. "

"Nonetheless, it is reasonable to suggest that some types of dietary FAs not only represent promising therapies for prevention and/or management of Her-2/neu-overexpressing breast carcinomas, but also may be even more beneficial when given in combination with novel therapies directed against Her-2/neu. We are currently investigating whether these findings will be helpful in the design of novel approaches to delay or prevent trastuzumab (Herceptin™) resistance. "

[R.B.]

Number of views 44,444

I just visited and saw this and it made me smile; I like patters in numbers, looking forward to 55,555

Thank you very much for your interest and support everybody

I have learned a lot in the process

[Andrea Barnett Budin]

Hi RB,

It's always good to feel appreciated for all your hard work and well-intentioned efforts! And that you are.

Plus, you're right, as we give we learn, and grow and that is the marvelous part of giving of yourself. It's a WIN WIN situation!!

Love,
Andi

[R.B.]

A bit complicated but yet more evidence of the involvement of Omega 6 in breast cancers.

D6D is one of the enzymes that convert plant based Omega 6 (LA) and plant based Omega 3 to the longer fats of the same respective families. The amount of Omega 3 or 6 stored in cell membranes ready for conversion by these enzymes is proportional to the dietary intake.

AA is a longer chain Omega 6.

PGE2 is an oxidized from of AA.

So it is possible to change the processes that take place in these pathways though the choice of dietary intakes of fats.

As often discussed in general on a population wide basis we eat far to much plant based Omega 6 (50% to 70% of many vegetable oils), and too little Omega 3 both plant based and long chain including EPA and DHA, which are not found in many food in quantity. etc etc.



Cancer Sci. 2013 Jun;104(6):760-4. doi: 10.1111/cas.12129. Epub 2013 Mar 19.
Delta-6-desaturase activity and arachidonic acid synthesis are increased in human breast cancer tissue.
Pender-Cudlip MC, Krag KJ, Martini D, Yu J, Guidi A, Skinner SS, Zhang Y, Qu X, He C, Xu Y, Qian SY, Kang JX.
Source

Laboratory for Lipid Medicine and Technology, Department of Medicine, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA.
Abstract

Omega-6 (n-6) arachidonic acid (AA) and its pro-inflammatory metabolites, including prostaglandin E2 (PGE(2)), are known to promote tumorigenesis. Delta-6 desaturase (D6D) is the rate-limiting enzyme for converting n-6 linoleic acid (LA) to AA. Our objective was to determine if AA synthesis, specifically D6D activity, and PGE(2) levels are increased in cancerous breast tissue, and whether these variables differ between estrogen receptor positive (ER+) and negative (ER-) breast cancers. Gas chromatography was performed on surgical breast tissue samples collected from 69 women with breast cancer. Fifty-four had ER+ breast cancer, and 15 had ER- breast cancer. Liquid chromatography-mass spectrometry was used to determine PGE(2) levels. Lipid analysis revealed higher levels of LA metabolites (C18:3 n-6, C20:3 n-6, and AA) in cancerous tissue than in adjacent noncancerous tissue (P < 0.01). The ratio of LA metabolites to LA, a measure of D6D activity, was increased in cancerous tissue, suggesting greater conversion of LA to AA (P < 0.001), and was higher in ER- than in ER+ patients, indicating genotype-related trends. Similarly, PGE(2) levels were increased in cancerous tissue, particularly in ER- patients. The results showed that the endogenous AA synthetic pathway, D6D activity, and PGE(2) levels are increased in breast tumors, particularly those of the ER- genotype. These findings suggest that the AA synthetic pathway and the D6D enzyme in particular may be involved in the pathogenesis of breast cancer. The development of drugs and nutritional interventions to alter this pathway may provide new strategies for breast cancer prevention and treatment.

OR eat much less Omega 6 and more Omega 3, a whole food diet that has not been de-mineralised and oxidised in storage and processing etc . . . but to give this advice would not be very helpful if your future career depended on securing future funding for drugs research. . . there has to be a better way of looking at health provision, a market that is more aware that we all share a very small precious planet, and will need to be at our best to have any hope of keeping it that way, that allows researchers to both secure research funding to expand important knowledge and give optimal health advice !

[R.B.]

Thing are rarely simple, and still much is unknown; the mysteries of estrogen !

N-3 Poly-Unsaturated Fatty Acids Shift Estrogen Signaling to Inhibit Human Breast Cancer Cell Growth

http://www.plosone.org/article/info%...l.pone.0052838

WenQing Cao, ZhiFan Ma, Mark M. Rasenick, ShuYan Yeh, JiangZhou Yu

"These findings may not only provide the evidence to link n-3 PUFAs biologic effects and the pro-apoptotic signaling of estrogen in breast cancer cells, but also shed new insight into the potential application of n-3 PUFAs in BCa treatment."


"Introduction

Fish oil dietary supplements have become increasingly popular. They are consumed for a variety of ailments as well as for promotion of general health. Population and preclinical studies have suggested that n-3 PUFAs inhibit BCa growth and improve treatment outcomes [1]. Accumulating evidence states that n-3 PUFAs may exert an antitumor action by altering lipid composition of the plasma membrane, which may affect the physical and chemical properties of lipid rafts, consequently, affecting localization of and interactions among signaling components in the microdomains of cell membrane [2]–[4]. Recent studies in breast cancer cells also found that, n-3 PUFA could incorporate different components of the cell membrane to remodel membrane architecture [5], [6]. These suggested a potential mechanism underlying n-3 PUFA anti-cancer effect. N-3 PUFA treatment decreases EGFR signaling [7], and down-regulates CXCR4 signaling in MDA-MB-231 cells [8], which might play the important roles in the anti-BCa effect of n-3 PUFAs. While E2 signaling is crucial for BCa tumorigenesis and progression, fewer studies have addressed how n-3 PUFAs affect E2 signaling and biologic function in BCa cells. It is noteworthy that in the animal studies on chemo-preventive properties of n-3 PUFAs, estrogen does not override the inhibitory effect of high n-3 PUFA diet on BCa growth [9], implying that n-3 PUFAs might abrogate/reduce/reverse the pro-proliferative effect of estrogen.

Estrogen, a mitogen, stimulates cell proliferation and prevents cell death in many different cell types, and is an important risk factor for BCa development [10]. Anti-estrogen therapies have been widely employed to treat hormone dependent BCa. However, laboratory studies have suggested that estrogen stimulates the apoptosis in long-term estrogen deprivation of MCF-7 BCa cells, and switches from being a mitogenic agent to inhibiting growth and inducing apoptosis [11]–[13]. Two potential mechanisms underlying this paradoxical effect of estrogen have been suggested in the studies that can be triggered either through the extrinsic death receptor pathway [12] or via the intrinsic pathway of mitochondrial disruption and release of cytochrome C [11]. Nevertheless, it is not clear how estrogen might promote BCa cell apoptosis.

Based on the above scientific findings, we propose that n-3 PUFAs alter estrogen signaling cascades in BCa cells, and initiate/augment the inhibitory effect of E2 (or compounds binding to membrane E2 receptors) on breast cancer. In this study, we first found that n-3 PUFA treatment initiated the inhibitory effect of E2 on MCF-7 and T47D BCa cell growth, and increased cell apoptosis. While these effects of estrogen were independent of the classical estrogen receptors, ERα or ERβ, they required the presence of the estrogen-sensitive G protein coupled receptor (GPCR), GPER1. Data from this study could lead to novel insights into the usefulness of n-3 PUFAs in the treatment of BCa."

[R.B.]

And just in case you missed this on the iodine thread on the nutrition page . . .

"And for all you reggae fans; something to listen to http://tonyvendryes.com/ whilst reading this thread (-:

(It takes a few seconds for the music to start once you the page opens, worth the wait )

Bear with the spoken intro (-:

Love the lyrics (-:

I have not looked at the site content, but love this Doctor's approach."

http://tonyvendryes.com/

"Prevention is better than cure you often have been told make wellness your number one goal for health is better than gold"

[Andrea Barnett Budin]

Love the music, the accent AND THE MESSAGE!

We are each a healer. We just have to awaken that part of ourselves.

Thanks, R.B.

[R.B.]

Both Omega 3 and calorie restriction have been suggested to have a role inhibiting cancers.

Here mice that over-express HER2 were allowed to eat as much as they wanted (AL), or calorie restricted. Some were fed with an omega 6 rich oil (soy oil which contains some plant based Omega 3 unlike many other vegetable oils) as their main fat and others with the Omega 3 EPA as their main fat.

The eat all you like high Omega 6 mice had an 87% tumor incidence, and the intermittently calorie restricted with a high Omega 3 EPA intake had a 15% tumor incidence, which is thought provoking as well as supporting the general contention of this thread.

It is interesting that intermittent calorie restriction was more effective than chronic restriction, which raises a lot of questions.

It would be interesting to know the original dietary content of the mice and their fat tissue compositions prior to the experiment; I have not seen the full paper.

As previously discussed on the separate but related topic of ketogenic diets for cancer, it is also likely that outcomes will depend on the type of fat consumed.

control (Con) ad libitum (AL),
intermittent calorie-restricted (ICR)
chronic calorie-restricted (CCR)




Cancer Prev Res (Phila). 2013 Jun;6(6):540-7. doi: 10.1158/1940-6207.CAPR-13-0033. Epub 2013 Apr 2.
Combination of intermittent calorie restriction and eicosapentaenoic acid for inhibition of mammary tumors.
Mizuno NK, Rogozina OP, Seppanen CM, Liao DJ, Cleary MP, Grossmann ME.
Author information
Abstract

There are a number of dietary interventions capable of inhibiting mammary tumorigenesis; however, the effectiveness of dietary combinations is largely unexplored. Here, we combined 2 interventions previously shown individually to inhibit mammary tumor development. The first was the use of the omega-3 fatty acid, eicosapentaenoic acid (EPA), and the second was the implementation of calorie restriction. MMTV-Her2/neu mice were used as a model for human breast cancers, which overexpress Her2/neu. Six groups of mice were enrolled. Half were fed a control (Con) diet with 10.1% fat calories from soy oil, whereas the other half consumed a diet with 72% fat calories from EPA. Within each diet, mice were further divided into ad libitum (AL), chronic calorie-restricted (CCR), or intermittent calorie-restricted (ICR) groups. Mammary tumor incidence was lowest in ICR-EPA (15%) and highest in AL-Con mice (87%), whereas AL-EPA, CCR-Con, CCR-EPA, and ICR-Con groups had mammary tumor incidence rates of 63%, 47%, 40%, and 59%, respectively. Survival was effected similarly by the interventions. Consumption of EPA dramatically reduced serum leptin (P < 0.02) and increased serum adiponectin in the AL-EPA mice compared with AL-Con mice (P < 0.001). Both CCR and ICR decreased serum leptin and insulin-like growth factor I (IGF-I) compared with AL mice but not compared with each other. These results illustrate that mammary tumor inhibition is significantly increased when ICR and EPA are combined as compared with either intervention alone. This response may be related to alterations in the balance of serum growth factors and adipokines.

[R.B.]

Nutr Cancer. 2014 Jan;66(1):68-76. doi: 10.1080/01635581.2014.847964. Epub 2013 Nov 25.
High-dose eicosapentaenoic Acid and docosahexaenoic Acid supplementation reduces bone resorption in postmenopausal breast cancer survivors on aromatase inhibitors: a pilot study.
Hutchins-Wiese HL, Picho K, Watkins BA, Li Y, Tannenbaum S, Claffey K, Kenny AM.
Author information
Abstract

Postmenopausal breast cancer survivors are living longer; however, a common class of drugs, aromatase inhibitors (AI), depletes estrogen levels, promotes bone loss, and heightens fracture risk. Eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) may offset AI effects to bone because of the known effects on cellular processes of bone turnover. Therefore, we hypothesized that 4 g of EPA and DHA daily for 3 mo would decrease bone turnover in postmenopausal breast cancer survivors on AI therapy in a randomized, double-blind, placebo controlled pilot study that included 38 women. At baseline and 3 mo, serum fatty acids, bone turnover, and inflammatory markers were analyzed. Serum EPA and DHA, total and long-chain (LC) omega (n)-3 polyunsaturated fatty acids (PUFA) increased, whereas arachidonic acid, total and LC n-6 PUFA, and the LC n-6:n-3 PUFA ratio decreased compared to placebo (all P < .05). Bone resorption was inhibited in the fish oil responders compared to placebo (P < .05). Inflammatory markers were not altered. This short-term, high-dose fish oil supplementation study's findings demonstrate that fish oil can reduce bone resorption; however, longer-term studies are needed to assess bone density preservation and to explore mechanistic pathways in this population at high risk for bone loss.

[R.B.]

More general advice on the importance of the Omega 3:6 ratio



http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3987049/


Helping women to good health: breast cancer, omega-3/omega-6 lipids, and related lifestyle factors
Michel de Lorgerilcorresponding author1 and Patricia Salen1
Author information ► Article notes ► Copyright and License information ►
Go to:
Abstract

In addition to genetic predisposition and sex hormone exposure, physical activity and a healthy diet play important roles in breast cancer (BC). Increased intake of omega-3 fatty acids (n-3) associated with decreased omega-6 (n-6), resulting in a higher n-3/n-6 ratio compared with the western diet, are inversely associated with BC risk, as shown by Yang et al. in their meta-analysis in BMC Cancer. High consumption of polyphenols and organic foods increase the n-3/n-6 ratio, and in turn may decrease BC risk. Intake of high fiber foods and foods with low glycemic index decreases insulin resistance and diabetes risk, and in turn may decrease BC risk. The modernized Mediterranean diet is an effective strategy for combining these recommendations, and this dietary pattern reduces overall cancer risk and specifically BC risk. High-risk women should also eliminate environmental endocrine disruptors, including those from foods. Drugs that decrease the n-3/n-6 ratio or that are suspected of increasing BC or diabetes risk should be used with great caution by high-risk women and women wishing to decrease their BC risk.

Please see related article: http://www.biomedcentral.com/1471-2407/14/105/abstract.

[R.B.]

And from the same authors the following heads up. I have not looked into statins in any detail so cannot meaningfully comment. There are suggestions that statins both increase and reduce cancer risk


http://www.ncbi.nlm.nih.gov/pubmed/24903828

BMC Med. 2014 Jun 5;12(1):94. doi: 10.1186/1741-7015-12-94.
Do statins increase and Mediterranean diet decrease the risk of breast cancer?
de Lorgeril M1, Salen P.
Author information
Abstract
BACKGROUND:

Physical exercise and healthy dietary habits are recommended to prevent breast cancer.
DISCUSSION:

Increased intake of omega-3 fatty acids associated with decreased omega-6 - resulting in higher omega-3 to omega-6 ratio compared with Western-type diet - is inversely associated with breast cancer risk. The modernized Mediterranean diet with high omega-3 to omega-6 ratio, high fiber and polyphenol intake, and consumption of low-glycemic index foods reduces overall cancer risk and specifically breast cancer risk. It has been suggested that consuming no more than one alcoholic drink per day, preferably wine, is preferable. Eliminating environmental contaminants, including endocrine disruptors, and favoring organic foods to increase polyphenol intake and the omega-3 to omega-6 ratios were also shown to be beneficial. Cholesterol-lowering statins may decrease antitumor defenses; are toxic for the mitochondria; decrease the omega-3 to omega-6 ratio; increase body mass index, insulin resistance and diabetic risk; and have been associated with an increased breast cancer risk.
SUMMARY:

Therefore, as well as making lifestyle changes to decrease breast cancer risk, we argue that physicians should carefully consider (and often avoid) therapies that may increase breast cancer or diabetes risk in high-risk women and women who wish to decrease their breast cancer risk

[SoCalGal]

Hi RB,
great info as always. one of my best docs has been talking about this for 7 years. It's why I'm gluten and dairy free and work hard to balance the omegas. He's also very down on statins as they are so widely prescribed. Luckily not an issue for me.
Thanks for the info - gonna copy and re-post on my Facebook feed!

[R.B.]

If anybody is in the UK and interested I am speaking at a Royal Society of Medicine food section conference on hidden nutritional deficiencies in my new role as recently appointed Chair of the McCarrison Society, which is a venerable society with its own widely recognized Journal 'Nutrition and Health'.

I will be looking in whistle-stop fashion at deficiencies in nutrients particularly Iodine, Vitamin D, minerals, and imbalances in Omega 3 and 6 set within the context of the shoreline diet which arguably provided the conditions for out existence.

The Society has a long illustrious history, but is in need of a bit of revamping including a new web site.

I am hoping to make it a forum to bring together the Food Agricultural and Health sectors to the same table, which they never are, to try and bring focus on deficiencies such as Vitamin D, Iodine and secure the implementation of strategies to address them.

This is the link to the conference.

http://www.rsm.ac.uk/events/fhf01

[R.B.]

GREAT to see the forum back

FREE STUDENT PLACES (UK accredited conference at the Royal Society of Medicine - food section)

There are a small number of free student (medical nutrition related) places at the above, but the offer closes tomorrow apparently. If interested please Pmail me

Availability depends on demand but I will be delighted to pass the application on.

The spaces have now gone - sorry about the previous typos - did not see them at the time

[R.B.]

18:3n3 is linolenic acid the plant based 18 carbon found for example in flaxseed oil

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2033520/

FREE FULL TEXT available


Br J Cancer. 1994 Aug;70(2):330-4.
alpha-Linolenic acid content of adipose breast tissue: a host determinant of the risk of early metastasis in breast cancer.
Bougnoux P1, Koscielny S, Chajès V, Descamps P, Couet C, Calais G.
Author information
Abstract

The association between the levels of various fatty acids in adipose breast tissue and the emergence of visceral metastases was prospectively studied in a cohort of 121 patients with an initially localised breast cancer. Adipose breast tissue was obtained at the time of initial surgery, and its fatty acid content analysed by capillary gas chromatography. A low level of alpha-linolenic acid (18:3n-3) in adipose breast tissue was associated with positive axillary lymph node status and with the presence of vascular invasion, but not with tumour size or mitotic index. After an average 31 months of follow-up, 21 patients developed metastases. Large tumour size, high mitotic index, presence of vascular invasion and low level of 18:3n-3 were single factors significantly associated with an increased risk of metastasis. A Cox proportional hazard regression model was used to identify prognostic factors. Low 18:3n-3 level and large tumour size were the two factors predictive of metastases. These results suggest that host alpha-linolenic acid has a specific role in the metastatic process in vivo. Further understanding of the biology of this essential fatty acid of the n-3 series is needed in breast carcinoma.

[R.B.]

Eur J Cancer. 2000 Feb;36(3):335-40.
Low alpha-linolenic acid content of adipose breast tissue is associated with an increased risk of breast cancer.
Klein V1, Chajès V, Germain E, Schulgen G, Pinault M, Malvy D, Lefrancq T, Fignon A, Le Floch O, Lhuillery C, Bougnoux P.
Author information
Abstract

Data derived from experimental studies suggest that alpha-linolenic acid may have a protective effect in breast cancer. Observations obtained from epidemiological studies have not allowed conclusions to be drawn about a potential protective effect of dietary alpha-linolenic acid on breast cancer, possibly because of methodological issues. This case-control study conducted in an homogeneous population from a central area in France was designed to explore the hypothesis that alpha-linolenic acid inhibits breast cancer, using fatty acid levels in adipose breast tissue as a biomarker of past qualitative dietary intake of fatty acids. Biopsies of adipose breast tissue at the time of diagnosis were obtained from 123 women with invasive non-metastatic breast carcinoma. 59 women with benign breast disease served as controls. Individual fatty acids were analysed by capillary gas chromatography. An unconditional logistic regression model was used to obtain odds ratio estimates whilst adjusting for age, menopausal status and body mass index (BMI). No association was found between fatty acids (saturates, monounsaturates, long-chain polyunsaturates n-6 or n-3) and the disease, except for alpha-linolenic acid which showed an inverse association with the risk of breast cancer. The relative risk of breast cancer for women in the highest quartile of adipose breast tissue alpha-linolenic acid level was 0.36 (95% confidence interval=0.12-1.02) compared with those in the lowest quartile (P trend=0.026), suggesting a protective effect of alpha-linolenic acid in the risk of breast cancer. The effects of dietary alpha-linolenic on the risk of breast cancer warrant further study.

[R.B.]

Hi All

Role of dietary fatty acids in mammary gland development and breast cancer


Definitely worth a quick skin or full read if you have the time.

Some general and understandable background into the role of Omega 6 and 3 on the risk of breast cancer set in the context of long term intakes.

I am sorry there have not been as many posts lately I have been really busy on related issues.

Hopefully you to will get full free access.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3096965/


Breast Cancer Res. 2010; 12(5): 211.
Published online 2010 Oct 26. doi: 10.1186/bcr2646
PMCID: PMC3096965
Role of dietary fatty acids in mammary gland development and breast cancer
Mira MacLennan and David WL Ma

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3096965/

[R.B.]

"Sugar in western diets increases risk for breast cancer tumors and metastasis"

"The high amounts of dietary sugar in the typical Western diet may increase the risk of breast cancer and metastasis to the lungs, according to a study at The University of Texas MD Anderson Cancer Center. "

http://medicalxpress.com/news/2016-0...st-cancer.html


What's this got to do with Omega 3 and 6 is probably your first thought.

A pathway increased by sugar is the expression of an enzyme called LOX12, which is an enzyme that is one of the key pathways by which plant based Omega 6 linoleic acid and the longer chain arachidonic acid are converted to downstream oxidized products that are highly bio-active including 12HETE, which has roles in controlling cell growth and invasion.

http://www.nature.com/bjc/journal/v1...c2011194a.html

The pathways are multiple and complex, and much remains to be determined, but several oxidized products of Omega 6s are associated with increased risks of cancer by multiple mechanisms.

So here it appears we have a cross amplification of relevant pathways by excess sugar and Omega 6s in the diet.

I see Lani has also posted the story. http://her2support.org/vbulletin/showthread.php?t=64352

This emphases how interlinked things are and that approaches need to be holistic.

[R.B.]

An ACSO meeting presentation Mediterranean Diet v Other Diet - 3 years - return of cancer - 0 v 11

I will go and try and find the paper at some point - the details of the diets would be interesting.

News paper report

Yes a small study number but nonetheless thought provoking.


http://www.theguardian.com/society/2...fish-olive-oil

"Mediterranean diet may help stop breast cancer coming back, study says "

Abstract


"The study presented at the American Society of Clinical Oncology (ASCO) meeting in Chicago is a trial in Italy which compared the outcomes for 307 women who had been treated for early breast cancer. One group of 199 women were asked to eat a Mediterranean diet, involving four portions of vegetables, three pieces of fruit and one serving of grains a day, together with four or more servings of fish each week, some red and processed meat and plenty of olive oil. They were allowed up to one alcoholic drink a day.

The other group of 108 women were asked to eat their normal diet, but given advice on healthy food by a dietician.

The cancer researchers at Piacenza hospital, Italy, found that after three years, 11 women from the group eating a normal diet suffered a return of their breast cancer, while none of those eating a Mediterranean diet did."

Another papers perspective

http://www.independent.co.uk/life-st...-a7066056.html